subject:(GDNF)

1. Roxo, Tiago Filipe Dias Santos. Efeito anti-inflamatório do GDNF: qual a sua contribuição para a neuroprotecção dopaminérgica?.

Degree: 2013, Universidade da Beira Interior

URL: https://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/1625

► Microglia are the resident macrophages of the Central Nervous System and act as the main form of immune defence. Microglia can assume an activated state… (more)

▼ Microglia are the resident macrophages of the Central Nervous System and act as the main form of immune defence. Microglia can assume an activated state in case of inflammation, having its phagocytic activity increased, also releasing reactive oxygen species, in order to protect the Central Nervous System cells from injury. However, activated microglia has also been associated with neurodegeneration. Increased interleukin and cytokine levels have been described in neurodegenerative diseases, namely Parkinson’s disease, where the loss of dopaminergic neurons has been related to excessive microglial activation. Soluble factors released by astrocytes are capable to modulate microglial reactivity. From these factors, glial cell line-derived neurotrophic factor (GDNF) stood out for its ability to protect dopaminergic neurons from injury, both in vitro an in vivo. Some studies have also demonstrated an anti-inflammatory action of GDNF, mediated by its receptor GFR1, suggesting that these two effects of GDNF may be related to each other. However, no study has provided a clear evidence for a cause-effect relationship between them. Therefore, this work aims at elucidating the importance of GDNF control of microglial reactivity to the survival of dopaminergic neurons. The main strategy will be to block the action of GDNF specifically in microglial cells, through GFR1 silencing, and to evaluate its effect on the neuroprotective action of GDNF in the presence of an inflammatory stimuli. The expression of GFR1 in primary ventral midbrain microglia and N9 microglia cell line cultures was confirmed through immunochemistry and Western Blot. Silencing of GFR1, through siRNA, in N9 microglia cells was successfully accomplished and preliminary results suggest that silencing of this receptor in primary cultures of microglia is also doable. Co-cultures of N9 microglia cells and neuron-glia mixed cultures were exposed to different concentrations of LPS which induced a selective dopaminergic injury. Under these conditions, an increase in microglial reactivity was observed. Additional experiments will be necessary to achieve the main goal of this work. However, these results will support future experiments in order to elucidate the relevance of the anti-inflammatory effect of GDNF on dopaminergic neuroprotection. Advisors/Committee Members: Fonseca, Carla Sofia Pais, Baltazar, Graça Maria Fernandes.

Subjects/Keywords: Microglia; GDNF; GDNF (GFRalfa1); Neurónios dopaminérgicos; Neurodegeneração

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Roxo, T. F. D. S. (2013). Efeito anti-inflamatório do GDNF: qual a sua contribuição para a neuroprotecção dopaminérgica?. (Thesis). Universidade da Beira Interior. Retrieved from https://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/1625

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Roxo, Tiago Filipe Dias Santos. “Efeito anti-inflamatório do GDNF: qual a sua contribuição para a neuroprotecção dopaminérgica?.” 2013. Thesis, Universidade da Beira Interior. Accessed January 18, 2021. https://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/1625.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Roxo, Tiago Filipe Dias Santos. “Efeito anti-inflamatório do GDNF: qual a sua contribuição para a neuroprotecção dopaminérgica?.” 2013. Web. 18 Jan 2021.

Vancouver:

Roxo TFDS. Efeito anti-inflamatório do GDNF: qual a sua contribuição para a neuroprotecção dopaminérgica?. [Internet] [Thesis]. Universidade da Beira Interior; 2013. [cited 2021 Jan 18]. Available from: https://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/1625.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Roxo TFDS. Efeito anti-inflamatório do GDNF: qual a sua contribuição para a neuroprotecção dopaminérgica?. [Thesis]. Universidade da Beira Interior; 2013. Available from: https://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/1625

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Queens University

2. Rodrigues, David. Glial Cell Line-Derived Neurotrophic Factor Modulates Structure and Function of Postnatal Myenteric Neurons .

Degree: Physiology, 2008, Queens University

URL: http://hdl.handle.net/1974/1396

► The enteric nervous system (ENS) continues its development after birth, with formation of ganglia and functional synapses; plasticity is also demonstrated in significant axon growth… (more)

▼ The enteric nervous system (ENS) continues its development after birth, with formation of ganglia and functional synapses; plasticity is also demonstrated in significant axon growth that occurs after experimental colitis in the adult colon. However, little is known about factors in the postnatal intestine that influence and regulate these processes. Therefore we tested the effects of known neurotrophins, NGF, NT-3, BDNF and GDNF on neonatal rat myenteric neurons. Cocultures were developed by isolating the myenteric plexus and surrounding muscular wall from neonatal rats, and effects of exogenous treatment of neurotrophins were analyzed using immunocytochemistry and image analysis. Western blotting and immunocytochemistry were performed to detect implicated neurotrophins and their receptors in the postnatal intestine. Functional aspects of effects of implicated neurotrophins were assessed by [3H]choline uptake and acetylcholine release in myenteric neurons. Last, TNBS-colitis was induced in adult rats to determine changes in GDNF secretion during the course of the disease. Application of 100ng/mL GDNF to a neonatal intestinal coculture containing neurons, glia and smooth muscle cells produced a 91.5% (p≤0.05) increase in axons. GDNF induced morphological changes in the structure and organization of neurons and axons; the incidence of neurons present in ganglia increased by 11.2% (p≤0.05), with a 32.9% (p≤0.05) increase in aggregated axons. Western blotting and immunocytochemistry confirmed intestinal smooth muscle as the major source of GDNF and demonstrated the presence of the GDNF receptor complex, GFRα1 and RET in the myenteric plexus. Choline uptake significantly increased at 50, 100 and 150ng/ml doses of GDNF, whereas stimulated ACh release increased only at 100 and 150ng/ml doses. In TNBS-colitis, a decrease in 35kD GDNF at days 1 and 6 post-induction of inflammation was observed, with a concomitant increase in 15kD GDNF. We conclude that GDNF, produced by intestinal smooth muscle, is a key factor influencing development of the postnatal myenteric neuron and may play a role in ENS-restructuring post-inflammation.

Subjects/Keywords: GDNF ; ENS

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Rodrigues, D. (2008). Glial Cell Line-Derived Neurotrophic Factor Modulates Structure and Function of Postnatal Myenteric Neurons . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/1396

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Rodrigues, David. “Glial Cell Line-Derived Neurotrophic Factor Modulates Structure and Function of Postnatal Myenteric Neurons .” 2008. Thesis, Queens University. Accessed January 18, 2021. http://hdl.handle.net/1974/1396.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Rodrigues, David. “Glial Cell Line-Derived Neurotrophic Factor Modulates Structure and Function of Postnatal Myenteric Neurons .” 2008. Web. 18 Jan 2021.

Vancouver:

Rodrigues D. Glial Cell Line-Derived Neurotrophic Factor Modulates Structure and Function of Postnatal Myenteric Neurons . [Internet] [Thesis]. Queens University; 2008. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1974/1396.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Rodrigues D. Glial Cell Line-Derived Neurotrophic Factor Modulates Structure and Function of Postnatal Myenteric Neurons . [Thesis]. Queens University; 2008. Available from: http://hdl.handle.net/1974/1396

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of New South Wales

3. Kaplinovsky, Tamila. The glial cell line-derived neurotrophic factor family in the olfactory system and brain.

Degree: Clinical School - St Vincent's Hospital, 2015, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/55676 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:38452/SOURCE02?view=true

► Glial cell line-derived neurotrophic factor (GDNF) family signaling hasbeen implicated in development, survival and function of many different celltypes, including neurons in the central nervous… (more)

▼ Glial cell line-derived neurotrophic factor (GDNF) family signaling hasbeen implicated in development, survival and function of many different celltypes, including neurons in the central nervous system. The family consists offour ligands [GDNF, neurturin (NTN), artemin and persephin] which bind to fourco-receptors (GFRα1-4) and recruit the tyrosine kinase receptor RET into thesignaling complex. In vivo, the ligands bind to the co-receptors with preferentialaffinity, e.g., GDNF to GFRα1 and NTN to GFRα2, whereas in vitro, cross-talkbetween the ligands and co-receptors has been demonstrated. RET exists astwo main alternatively spliced isoforms, RET9 and RET51. These isoforms differin their carboxyl termini and have been implicated with distinct functions in theenteric and central nervous systems. Clinically, GDNF and NTN have beenexamined as potential therapeutic agents for treatment of neurodegenerativedisorders, particularly Parkinson’s disease (PD), as these proteins were foundto provide essential trophic support to dopaminergic (DA) neurons, one of themain neuronal populations affected by this pathology. To progress developmentof such therapies further, a greater understanding of GDNF family signaling isnecessary, which was the aim of the current work.Two regions of the brain were studied – the olfactory system, a uniqueregion of the nervous system that supports lifelong neurogenesis; and thesubstantia nigra (SN), the site of DA neuron degeneration in PD. Expression ofGDNF, NTN, GFRα1 and GFRα2 was previously characterized in the olfactorysystem (Maroldt et al., 2005; Kaplinovsky and Cunningham, 2011). The currentwork specifically focused on expression of the RET isoforms in this system.Double-labeling fluorescent immunohistochemistry in vivo and in an olfactorycell culture model illustrated RET9 to be the predominantly expressed isoformin a pattern similar to the previously reported expression for GDNF and GFRα2.RET51 was generally expressed in a subset of RET9-positive cells and in vivo2restricted to the same region as NTN. Treatment of the olfactory cultures withGDNF initiated a strong neurogenerative response, potentially by acting on theGFRα2/RET9 signaling complex. NTN exposure promoted olfactory progenitorproliferation, again potentially via the GFRα2/RET9 signaling complex, as well asdifferentiation towards a nestin-positive non-neuronal lineage, speculated to besustentacular or olfactory ensheathing cells. The differentiating affect may havebeen propagated by GFRα1/RET51 as these proteins were expressed in thesame cells in culture.In the adult rat and human SN, RET9 was again found to be the predominantlyexpressed isoform, localized to all DA neurons, even in PD pathology. RET51was expressed in a subset of RET9-positive DA neurons in the rat. In humantissue, this isoform was virtually absent from healthy SN whereas in PD, astrong up-regulation was noted in DA neurons as well as s100B-positive glia.The results of this study demonstrate several important features regarding GDNFfamily signaling mechanisms.… Advisors/Committee Members: Shine, John, Clinical School - St Vincent's Hospital, Faculty of Medicine, UNSW, Doyle, Kharen, Clinical School - St Vincent's Hospital, Faculty of Medicine, UNSW.

Subjects/Keywords: Parkinson's Disease; GDNF; RET

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kaplinovsky, T. (2015). The glial cell line-derived neurotrophic factor family in the olfactory system and brain. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/55676 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:38452/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Kaplinovsky, Tamila. “The glial cell line-derived neurotrophic factor family in the olfactory system and brain.” 2015. Doctoral Dissertation, University of New South Wales. Accessed January 18, 2021. http://handle.unsw.edu.au/1959.4/55676 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:38452/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Kaplinovsky, Tamila. “The glial cell line-derived neurotrophic factor family in the olfactory system and brain.” 2015. Web. 18 Jan 2021.

Vancouver:

Kaplinovsky T. The glial cell line-derived neurotrophic factor family in the olfactory system and brain. [Internet] [Doctoral dissertation]. University of New South Wales; 2015. [cited 2021 Jan 18]. Available from: http://handle.unsw.edu.au/1959.4/55676 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:38452/SOURCE02?view=true.

Council of Science Editors:

Kaplinovsky T. The glial cell line-derived neurotrophic factor family in the olfactory system and brain. [Doctoral Dissertation]. University of New South Wales; 2015. Available from: http://handle.unsw.edu.au/1959.4/55676 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:38452/SOURCE02?view=true

University of Guelph

4. Toms, Derek Douglas. Involvement of GDNF and microRNA-378 in the regulation of porcine follicle maturation.

Degree: PhD, Department of Animal and Poultry Science, 2014, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/8305

► Within the developing antral follicle, several factors are required for successful maturation of both the oocyte and the granulosa cells. It has been repeatedly shown… (more)

▼ Within the developing antral follicle, several factors are required for successful maturation of both the oocyte and the granulosa cells. It has been repeatedly shown that oocytes isolated from smaller follicles have considerably less developmental potential than those isolated from more mature, large follicles, despite both types typically being capable of resuming meiosis. Research in our laboratory has previously identified glial cell line-derived neurotrophic factor (GDNF) as an important intraovarian factor that can improve oocyte development and embryo potential of both small and large follicle-derived oocytes when included in in vitro maturation (IVM) media. This thesis examined the transcriptomic changes that occur within the oocyte when cultured in the absence or presence of GDNF and how these relate to the size of the follicle from which the oocyte originates. This research was undertaken using a microarray specific to porcine oocytes and early embryos. We found that GDNF made the transcriptome of small follicle-derived oocytes more similar to that of large follicle-derived oocytes. Additionally, the expression of many genes in response to GDNF was found to have significant follicle size-dependent effects. We also examined the role of microRNAs (miRNAs) in follicular development by examining potential regulatory mechanisms on GDNF and progesterone receptor (PGR). While no significant miRNA-mediated inhibition of GDNF expression was found, we did establish a role for miR-378 in regulating PGR. The transcription factor activity of PGR regulates a number of gene products that are necessary for remodeling the follicular extracellular matrix and for releasing cytokines. Over expression of miR-378 decreased mRNA and protein levels of PGR, and congruently mRNA levels of several genes known to be regulated by PGR and important for follicular development. Interestingly, not only did miR-378 regulate expression of PGR, this miRNA was itself regulated by the pituitary hormone follicle-stimulating hormone (FSH). Taken together, we found that FSH mediates follicular differentiation by regulating expression of PGR, at least in part via the down regulation of miR-378. In examining the role of GDNF and miR-378 in cells of the antral follicle, this thesis has provided additional information for the mechanisms involved in follicle maturation. Both GDNF and miR-378 regulate important developmental processes that are necessary for successful follicle development to produce competent oocytes. As many species, including humans, have a limited pool of large, fully developed follicles understanding the mechanisms that increase oocyte developmental competence will be important for the advancement of assisted reproductive technologies. Advisors/Committee Members: Li, Julang (advisor).

Subjects/Keywords: GDNF; granulosa cells; microRNA-378; ovary; pig

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Toms, D. D. (2014). Involvement of GDNF and microRNA-378 in the regulation of porcine follicle maturation. (Doctoral Dissertation). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/8305

Chicago Manual of Style (16^th Edition):

Toms, Derek Douglas. “Involvement of GDNF and microRNA-378 in the regulation of porcine follicle maturation.” 2014. Doctoral Dissertation, University of Guelph. Accessed January 18, 2021. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/8305.

MLA Handbook (7^th Edition):

Toms, Derek Douglas. “Involvement of GDNF and microRNA-378 in the regulation of porcine follicle maturation.” 2014. Web. 18 Jan 2021.

Vancouver:

Toms DD. Involvement of GDNF and microRNA-378 in the regulation of porcine follicle maturation. [Internet] [Doctoral dissertation]. University of Guelph; 2014. [cited 2021 Jan 18]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/8305.

Council of Science Editors:

Toms DD. Involvement of GDNF and microRNA-378 in the regulation of porcine follicle maturation. [Doctoral Dissertation]. University of Guelph; 2014. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/8305

5. Roam, Jacob. Growth Factor Gradient Formation and Release from PEG Microspheres for Nerve Regeneration.

Degree: PhD, Biomedical Engineering, 2015, Washington University in St. Louis

URL: https://openscholarship.wustl.edu/eng_etds/116

► Many biological processes depend on concentration gradients in signaling molecules. Thus, introduction of spatial patterning of proteins, while retaining activity and releasability, will be… (more)

▼ Many biological processes depend on concentration gradients in signaling molecules. Thus, introduction of spatial patterning of proteins, while retaining activity and releasability, will be critical for the field of regenerative medicine. In particular, the area of nerve regeneration is in need of innovations to improve outcomes. Only about 25% of surgical patients with peripheral nerve damage (~200,000 surgical interventions performed each year) regain full motor function with less than 3% regaining sensation. The use of nerve guidance conduits (NGC’s) which are filled with biomimetic scaffolds is one treatment being explored. These scaffolds, however, lack the spatial patterning of proteins found in native tissue. Glial-cell line derived neurotrophic factor (GDNF), a potent stimulator of axon regeneration, is one such protein that, if contained within the scaffold and conformed to a particular concentration profile, could greatly enhance neural regeneration. The object of this work is to utilize poly(ethylene glycol) (PEG) microspheres to accomplish this spatial patterning of GDNF and apply it to NGC’s. First, an approach utilizing the controllability of the PEG microsphere’s density (buoyancy) was explored. By creating the microspheres under varying conditions, incubation time and temperature, the cross-linking and, thus, the swelling rate of the microspheres could be controlled. This created microspheres of different densities that, upon centrifugation, would orient themselves within a scaffold, creating a gradient in the different microsphere types. GDNF loaded into a batch of microspheres would thusly be oriented within the scaffold along with that particular microsphere batch. Through this, gradients in GDNF were created. Heparin was also added to the microspheres to allow for reversible binding of GDNF. Next, gradients in reversibly bound GDNF were formed through sequential centrifugation of microsphere batches. For instance, a layer of GDNF loaded microspheres were formed into a scaffold followed by a layer of microspheres without GDNF on top of them. This created an initial step gradient in GDNF that, given time to release, would form a linear concentration gradient. Gradients formed by this method were visualized by fluorescent confocal microscopy and compared to Fickian models. Some conditions yielded profiles more linear than the model predictions, which persisted for over a week. Lastly, the sequential gradient formation was modified and applied to NGC’s. Before the scaffolds were ready for in vivo implantation, functionalities such as cell initiated degradability, cell adhesion, and inter-microsphere cross-linking were added. A plasmin degradable peptide sequence (GCGGVRNGGK) was incorporated into the microspheres. CLICK agents, laminin, and heparin (via a new binding chemistry) were attached to the microspheres to add inter-microsphere cross-linking, add cell adhesion, and heparin binding functionalities, respectively. GDNF gradient formation and activity retention were confirmed… Advisors/Committee Members: Donald L Elbert, Shelly Sakiyama-Elbert, Matthew Wood, Dennis Barbour, Jin-Yu Shao.

Subjects/Keywords: degradable; GDNF; gradient; heparin; NGC; PEG; Engineering

11 more images…

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Roam, J. (2015). Growth Factor Gradient Formation and Release from PEG Microspheres for Nerve Regeneration. (Doctoral Dissertation). Washington University in St. Louis. Retrieved from https://openscholarship.wustl.edu/eng_etds/116

Chicago Manual of Style (16^th Edition):

Roam, Jacob. “Growth Factor Gradient Formation and Release from PEG Microspheres for Nerve Regeneration.” 2015. Doctoral Dissertation, Washington University in St. Louis. Accessed January 18, 2021. https://openscholarship.wustl.edu/eng_etds/116.

MLA Handbook (7^th Edition):

Roam, Jacob. “Growth Factor Gradient Formation and Release from PEG Microspheres for Nerve Regeneration.” 2015. Web. 18 Jan 2021.

Vancouver:

Roam J. Growth Factor Gradient Formation and Release from PEG Microspheres for Nerve Regeneration. [Internet] [Doctoral dissertation]. Washington University in St. Louis; 2015. [cited 2021 Jan 18]. Available from: https://openscholarship.wustl.edu/eng_etds/116.

Council of Science Editors:

Roam J. Growth Factor Gradient Formation and Release from PEG Microspheres for Nerve Regeneration. [Doctoral Dissertation]. Washington University in St. Louis; 2015. Available from: https://openscholarship.wustl.edu/eng_etds/116

6. Fonseca, Ana Paula da Silva. Contribuição do GDNF para a neuroprotecção exercida pelo estrogénio:.

Degree: 2010, Universidade da Beira Interior

URL: http://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/799

► A doença de Parkinson é a segunda doença neurodegenerativa mais comum, depois do Alzheimer, e caracteriza-se principalmente pela perda progressiva de neurónios dopaminérgicos na Substantia… (more)

▼ A doença de Parkinson é a segunda doença neurodegenerativa mais comum, depois do Alzheimer, e caracteriza-se principalmente pela perda progressiva de neurónios dopaminérgicos na Substantia Nigra. Numerosos trabalhos reportaram a maior prevalência e incidência desta doença no sexo masculino, relativamente ao sexo feminino. Estudos envolvendo a reposição com estrogénios em ratos fêmea ovariectomizados, atribuíram esta diferença de incidências ao efeito neuroprotectivo do estrogénio. No entanto, o grau de protecção exercida por níveis fisiológicos desta hormona permanece desconhecido. Os estrogénios também têm sido implicados na regulação da expressão de factores neurotróficos, o que pode estar na origem dos seus efeitos neuroprotectores. O factor neurotrófico derivado de uma linha de células da glia (GDNF) é um dos factores neurotróficos regulados pelo estrogénio, que foi implicado na neuroprotecção e regeneração na via nigroestriatal, actuando como um potente factor de sobrevivência para os neurónios dopaminérgicos, que são alvo de degeneração na doença de Parkinson. De forma a esclarecer o papel dos níveis endógenos de estrogénio na protecção da via nigroestriatal, utilizámos como modelo da doença de Parkinson a 6-hidroxidopamina, e estudámos de que forma a remoção dos ovários em fêmeas férteis interferiu com a extenção da lesão dopaminérgica induzida pela toxina. As fêmeas Wistar foram ovariectomizadas e 3 semanas após a cirurgia os animais foram injectados estereotaxicamente, no estriado, com 6-hidroxidopamina. A extensão da lesão foi avaliada através da contagem de células que expressavam o marcador dopaminérgico tirosina hidroxilase, por imunohistoquimica, assim como pelos níveis de expressão desta proteína, por western blot, tanto na Substantia Nigra como no estriado. Os níveis plasmáticos de estradiol também foram quantificados. De forma a determinar a a existência de relação entre os níveis de estradiol, a expressão de GDNF e a extensão da lesão dopaminérgica, também foi estudada a expressão do factor neurotrófico GDNF. Os nossos resultados sugerem fortemente que o estrogénio produzido endogenamente, assim como o GDNF, estão associados com níveis aumentados de tirosina hidroxilase estriatal, um marcador de sobrevivência da célula dopaminérgica. Advisors/Committee Members: Baltazar, Graça Maria Fernandes.

Subjects/Keywords: Estrogénios; Estrogénios - Factor neurotrófico - GDNF; Estrogénios - Neuroprotecção - GDNF; Estrogénios - Doença de Parkinson

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Fonseca, A. P. d. S. (2010). Contribuição do GDNF para a neuroprotecção exercida pelo estrogénio:. (Thesis). Universidade da Beira Interior. Retrieved from http://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/799

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Fonseca, Ana Paula da Silva. “Contribuição do GDNF para a neuroprotecção exercida pelo estrogénio:.” 2010. Thesis, Universidade da Beira Interior. Accessed January 18, 2021. http://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/799.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Fonseca, Ana Paula da Silva. “Contribuição do GDNF para a neuroprotecção exercida pelo estrogénio:.” 2010. Web. 18 Jan 2021.

Vancouver:

Fonseca APdS. Contribuição do GDNF para a neuroprotecção exercida pelo estrogénio:. [Internet] [Thesis]. Universidade da Beira Interior; 2010. [cited 2021 Jan 18]. Available from: http://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/799.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Fonseca APdS. Contribuição do GDNF para a neuroprotecção exercida pelo estrogénio:. [Thesis]. Universidade da Beira Interior; 2010. Available from: http://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/799

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

7. Oliveira, Julieta Conceição Mendes Borges. GDNF e GPER: novas ferramentas no controlo da neuroinflamação?.

Degree: 2013, Universidade da Beira Interior

URL: http://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/1628

► As células microgliais, os macrófagos residentes no sistema nervoso central, são responsáveis pela resposta imune inata. Quando são moderadamente ativadas, realizam funções vitais, fagocitando células… (more)

▼ As células microgliais, os macrófagos residentes no sistema nervoso central, são responsáveis pela resposta imune inata. Quando são moderadamente ativadas, realizam funções vitais, fagocitando células mortas e removendo detritos celulares e toxinas. No entanto, uma ativação persistente destas células pode resultar numa desregulação da sua atividade. Elas podem tornar-se reativas e contribuir para a morte neuronal. Evidências crescentes sugerem que a inflamação e o stress oxidativo mediado pela microglia reativa desempenham um papel fundamental na progressão de várias doenças neurodegenerativas, como a doença de Parkinson. Tanto o fator neurotrófico derivado de uma linha de células da glia (GDNF) como os estrogénios são relatados por atuar na microglia, controlando a sua ativação excessiva. Um estudo anterior do nosso grupo mostrou que o GDNF presente em meio condicionado de astrócitos consegue inibir a reatividade microglial induzida pelo Zymozan A numa cultura primária de microglia do mesencéfalo ventral. O primeiro objetivo do presente trabalho foi o de verificar se a presença de neurónios, lesados ou não, poderia influenciar este efeito anti-inflamatório exercido pelo GDNF. Utilizando o mesmo tipo de cultura verificámos que o condicionamento na presença de neurónios reverteu a inibição da produção de NO exercida pelos meios condicionados apenas por astrócitos na microglia estimulada com LPS. Este diferente efeito dos dois meios poderá estar relacionado com o facto de os meios condicionados por culturas mistas de neurónios e astrócitos apresentaram níveis mais baixos de GDNF que os meios condicionados apenas por astrócitos. Por outro lado, estudos utilizando culturas primárias de microglia, bem como linhas celulares, demonstraram a capacidade do estrogénio para atenuar a ativação da microglia, em termos de atividade fagocítica, produção de espécies reativas de oxigénio e de azoto, bem como de outros fatores da cascata inflamatória. Está já descrita a capacidade dos estrogénios ativarem os recetores de estrogénio α e β presentes na microglia. No entanto, mais recentemente identificou-se um recetor de estrogénios transmembranar, o recetor de estrogénio acoplado à proteína G (GPER). O segundo objetivo do trabalho foi esclarecer a participação do GPER no controle da reatividade microglial mediada pelo estradiol. Utilizando uma linha celular de microglia N9, um agonista e um antagonista seletivos do recetor, verificamos que a ativação do GPER promoveu a migração das células microgliais e reduziu significativamente os parâmetros de reatividade microglial estudados. Estes resultados sugerem que o GPER pode ser um importante alvo terapêutico para doenças neurodegenerativas e neuroinflamatórias, especialmente nos homens, nos quais a terapia com estrogénio não é viável. Advisors/Committee Members: Baltazar, Graça Maria Fernandes, Fonseca, Carla Sofia Pais.

Subjects/Keywords: Doença neurodegenerativa; Microglia; Astrócitos - Actividade microglial - GDNF; Estrogénios - Actividade microglial - GDNF; Estrogénios - Actividade microglial - GPER; Neuroinflamação

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Oliveira, J. C. M. B. (2013). GDNF e GPER: novas ferramentas no controlo da neuroinflamação?. (Thesis). Universidade da Beira Interior. Retrieved from http://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/1628

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Oliveira, Julieta Conceição Mendes Borges. “GDNF e GPER: novas ferramentas no controlo da neuroinflamação?.” 2013. Thesis, Universidade da Beira Interior. Accessed January 18, 2021. http://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/1628.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Oliveira, Julieta Conceição Mendes Borges. “GDNF e GPER: novas ferramentas no controlo da neuroinflamação?.” 2013. Web. 18 Jan 2021.

Vancouver:

Oliveira JCMB. GDNF e GPER: novas ferramentas no controlo da neuroinflamação?. [Internet] [Thesis]. Universidade da Beira Interior; 2013. [cited 2021 Jan 18]. Available from: http://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/1628.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Oliveira JCMB. GDNF e GPER: novas ferramentas no controlo da neuroinflamação?. [Thesis]. Universidade da Beira Interior; 2013. Available from: http://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/1628

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Helsinki

8. Nuotio, Ulpukka. Characterization of small molecule GDNF family ligand mimetic BT44 for the treatment of neuropathic pain.

Degree: Department of Food and Environmental Sciences; Helsingfors universitet, Agrikultur- och forstvetenskapliga fakulteten, Institutionen för livsmedels- och miljövetenskaper, 2017, University of Helsinki

URL: http://hdl.handle.net/10138/191288

► Neuropathic pain is pain caused by injury or damage to the nervous system. This adverse condition affects millions of people in all parts of the… (more)

▼ Neuropathic pain is pain caused by injury or damage to the nervous system. This adverse condition affects millions of people in all parts of the world, and no known cure has been developed. Existing treatments are mainly anti-depressants or opioids that alleviate symptoms instead of repairing damaged neurons. Glial cell line-derived neurotrophic factor (GDNF) and artemin, belonging to GDNF family ligands, have been shown to restore damaged neurons. However due to the poor pharmaceutical properties of these proteins, such as difficult administration and expensive production, their transition to clinics is complicated. That is why we have been developing small molecule GFL-mimetics as an alternative. One of these mimetics is a compound named BT44. Characterization of BT44 began with in vitro experiments, where we tested the compound’s ability to activate luciferase reporter gene in cells expressing GDNF (GFRalpha1 and RET) and artemin (GFRalpha3 and RET) receptors, as well as ability to induce RET phosphorylation and activate intracellular MAPK/ERK and Pi3-K/Akt pathways. Furthermore, we tested stimulation of neurite outgrowth by the compound from cultured dorsal root ganglion neurons. In a similar manner to GDNF and artemin, BT44 was shown to activate GFRalpha1/RET and GFRalpha3/RET receptors and induce RET phosphorylation and intracellular signaling, in addition to stimulating neurite outgrowth from cultured DRG neurons. Because of the promising in vitro results, we moved on to in vivo testing in rat spinal nerve ligation (SNL) model of neuropathic pain. Similarly to artemin, BT44 was able to alleviate mechanical nociception and cold allodynia in SNL rats. In addition, we found that BT44 normalized to a certain degree nociception-related markers influenced by SNL in the tissues of experimental animals, which emulates previously published results for artemin. To summarize, our results indicate that BT44 is effective in neuronal restoration and pain alleviation, suggesting it for further development as innovative neuropathic pain treatment.

Subjects/Keywords: GDNF; neuropathic pain; pain treatment; GDNF family ligands; artemin; mimetics; Bioteknik (EYT); Biotechnology (EYT); Biotekniikka (EYT)

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Nuotio, U. (2017). Characterization of small molecule GDNF family ligand mimetic BT44 for the treatment of neuropathic pain. (Masters Thesis). University of Helsinki. Retrieved from http://hdl.handle.net/10138/191288

Chicago Manual of Style (16^th Edition):

Nuotio, Ulpukka. “Characterization of small molecule GDNF family ligand mimetic BT44 for the treatment of neuropathic pain.” 2017. Masters Thesis, University of Helsinki. Accessed January 18, 2021. http://hdl.handle.net/10138/191288.

MLA Handbook (7^th Edition):

Nuotio, Ulpukka. “Characterization of small molecule GDNF family ligand mimetic BT44 for the treatment of neuropathic pain.” 2017. Web. 18 Jan 2021.

Vancouver:

Nuotio U. Characterization of small molecule GDNF family ligand mimetic BT44 for the treatment of neuropathic pain. [Internet] [Masters thesis]. University of Helsinki; 2017. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10138/191288.

Council of Science Editors:

Nuotio U. Characterization of small molecule GDNF family ligand mimetic BT44 for the treatment of neuropathic pain. [Masters Thesis]. University of Helsinki; 2017. Available from: http://hdl.handle.net/10138/191288

Queens University

9. Kearon, Joanne. Selective damage to and protection of enteric neurons in vitro in models of ischemia and reperfusion .

Degree: Neuroscience Studies, 2014, Queens University

URL: http://hdl.handle.net/1974/12363

► The dysregulation of motility typical in inflammatory bowel disease (IBD) indicates involvement of the enteric nervous system (ENS). Indeed, animal models of IBD have demonstrated… (more)

▼ The dysregulation of motility typical in inflammatory bowel disease (IBD) indicates involvement of the enteric nervous system (ENS). Indeed, animal models of IBD have demonstrated that intestinal inflammation is typified by the early loss of enteric neurons. It has been proposed that ischemia may occur in intestinal inflammation, due to the organization of splanchnic circulation combined with local inflammatory damage. Therefore, we hypothesized that the ENS experiences ischemic challenge in inflammation, which we investigated by probing for hypoxia-inducible factor 1-α (HIF1-α) in the 2, 4, 6-trinitrobenzene sulfonic acid (TNBS)-model of colitis in adult rats. By Day 2 of TNBS-induced colitis, HIF1-α presence in the nuclei of myenteric neurons had significantly increased, indicating hypoxic challenge. Despite the potential for ischemia to occur in inflammation, little is known about the impact of the resultant metabolic inhibition on enteric neurons. We further hypothesized that metabolic challenge would cause neuronal damage. Glucose deprivation, hypoxia and treatment with an electron transport chain (ETC) uncoupler caused neuron loss and axonal damage in in vitro co-cultures of myenteric neurons, intestinal smooth muscle cells and glia. Furthermore, we investigated the potential impact of subsequent reperfusion on myenteric neurons by resupplying glucose following a period of deprivation. Resupply of glucose was observed to cause acute neuron loss in vitro. Lastly, if the ENS is damaged by ischemia and ischemia-reperfusion, it is then important to investigate methods of neuroprotection. In the CNS, glial cell line-derived neurotrophic factor (GDNF) and HIF1-α have both been demonstrated to be neuroprotective during metabolic inhibition. In co-cultures, GDNF was observed to prevent neuron loss by an ETC uncoupler or glucose deprivation. Hypoxic preconditioning also protected against neuron damage in a HIF1- α dependent manner. We concluded that the ENS is vulnerable to ischemia and ischemia-reperfusion occurring in inflammation. Further, GDNF and HIF1-α can be neuroprotective during metabolic challenge.

Subjects/Keywords: Enteric ; Inflammation ; Hypoxia ; Neurons ; GDNF ; Ischemia ; ENS ; Reperfusion

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kearon, J. (2014). Selective damage to and protection of enteric neurons in vitro in models of ischemia and reperfusion . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/12363

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Kearon, Joanne. “Selective damage to and protection of enteric neurons in vitro in models of ischemia and reperfusion .” 2014. Thesis, Queens University. Accessed January 18, 2021. http://hdl.handle.net/1974/12363.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Kearon, Joanne. “Selective damage to and protection of enteric neurons in vitro in models of ischemia and reperfusion .” 2014. Web. 18 Jan 2021.

Vancouver:

Kearon J. Selective damage to and protection of enteric neurons in vitro in models of ischemia and reperfusion . [Internet] [Thesis]. Queens University; 2014. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1974/12363.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Kearon J. Selective damage to and protection of enteric neurons in vitro in models of ischemia and reperfusion . [Thesis]. Queens University; 2014. Available from: http://hdl.handle.net/1974/12363

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Saskatchewan

10. Shen, Luping. The effects of fluoxetine and quetiapine on the proliferation and differentiation of, and GDNF release from, C6 cells.

Degree: 2006, University of Saskatchewan

URL: http://hdl.handle.net/10388/etd-04102006-120117

► According to the literature, there is a decrease in glial cell number or hypofunction of glial cells in depression. It was also found that both… (more)

▼ According to the literature, there is a decrease in glial cell number or hypofunction of glial cells in depression. It was also found that both antidepressants and atypical antipsychotics might target glial cells, and that they increase the release of glial-cell-line-derived neurotrophic factor (GDNF) from C6 rat glioma cells (C6 cells). In this project, C6 cells were used as a model for glial cells to investigate the effects of fluoxetine and quetiapine on proliferation and differentiation, and to investigate their effects on the release of GDNF. A combination of quetiapine and fluoxetine was used to study their potential synergistic effect on the release of GDNF from C6 cells. C6 cells were treated with different concentrations of fluoxetine and quetiapine in both normal and serum starvation culture conditions. Under the serum present condition, fluoxetine (25 mM) decreased the number of C6 cells from 24 to 48 h, while quetiapine (25 mM) decreased the cell number only at 48h. Under serum starvation, it was found that fluoxetine (12.5 mM) increased the number of C6 cells from 24 to 48 h treatment; in contrast, quetiapine (25 mM) decreased the number of C6 cells after 48 h treatment. Both fluoxetine and quetiapine inhibited the proliferation of C6 cells under normal and serum starvation conditions. Fluoxetine (12.5 mM) decreased C6 cell death, while quetiapine had no significant effect. Fluoxetine, but not quetiapine, changed the morphology of C6 cells and increased the level of glial fibrillary acidic protein (GFAP), an astrocyte marker. Both fluoxetine (12.5, 25 mM) and quetiapine (25 mM) increased the release of GDNF from C6 cells, and an apparent additive effect was found between quetiapine and fluoxetine in the modulation of release of GDNF from these cells. It was concluded that:1. High concentration (25 mM) of fluoxetine and quetiapine decreased the number of C6 cells under the serum present condition and both drugs inhibited the proliferation of C6 cells.2. Fluoxetine had a protective effect on the C6 cells under serum starvation, and affected the differentiation of C6 cells; this implies that fluoxetine may protect glial cells in vivo and affect their differentiation. 3. A high concentration of quetiapine decreased the number of C6 cells and inhibited the proliferation under serum starvation; even though it increased the release of GDNF from C6 cells as did fluoxetine.4. Both quetiapine and fluoxetine increased the release of GDNF from C6 cells under serum starvation. The combination of quetiapine and fluoxetine had an apparent additive effect in the modulation of GDNF release.5. These effects on proliferation & GDNF release may underlie the benefit observed with these drugs in treating depression and schizophrenia. Advisors/Committee Members: Dyck, Lillian E., Tuchek, John M., Mousseau, Darrell D., Li, Xin-Min.

Subjects/Keywords: GDNF quetiapine fluoxetine C6 cells

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Shen, L. (2006). The effects of fluoxetine and quetiapine on the proliferation and differentiation of, and GDNF release from, C6 cells. (Thesis). University of Saskatchewan. Retrieved from http://hdl.handle.net/10388/etd-04102006-120117

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Shen, Luping. “The effects of fluoxetine and quetiapine on the proliferation and differentiation of, and GDNF release from, C6 cells.” 2006. Thesis, University of Saskatchewan. Accessed January 18, 2021. http://hdl.handle.net/10388/etd-04102006-120117.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Shen, Luping. “The effects of fluoxetine and quetiapine on the proliferation and differentiation of, and GDNF release from, C6 cells.” 2006. Web. 18 Jan 2021.

Vancouver:

Shen L. The effects of fluoxetine and quetiapine on the proliferation and differentiation of, and GDNF release from, C6 cells. [Internet] [Thesis]. University of Saskatchewan; 2006. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10388/etd-04102006-120117.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Shen L. The effects of fluoxetine and quetiapine on the proliferation and differentiation of, and GDNF release from, C6 cells. [Thesis]. University of Saskatchewan; 2006. Available from: http://hdl.handle.net/10388/etd-04102006-120117

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

11. Gama, Susana Martins. Expressão de GDNF em células estriatais: efeito de fatores solúveis libertados por células do mesencéfalo ventral após lesão dopaminérgica.

Degree: 2012, RCAAP

URL: http://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/2864

► A doença de Parkinson (DP) é uma doença neurodegenerativa caracterizada pela degeneração progressiva dos neurónios dopaminérgicos (DA) que projetam da substantia nigra (SN) pars compacta… (more)

▼ A doença de Parkinson (DP) é uma doença neurodegenerativa caracterizada pela degeneração progressiva dos neurónios dopaminérgicos (DA) que projetam da substantia nigra (SN) pars compacta para o estriado, o que leva à redução dos níveis de dopamina nesta região encefálica. A principal abordagem terapêutica no tratamento da DP é a reposição da dopamina na forma do seu precursor L-3,4-dihidroxifenilalanina (L-DOPA). Embora esta terapia controle os sintomas nos estágios iniciais da doença, não é curativa e pode originar efeitos secundários. O uso de fatores neurotróficos pode ser uma estratégia terapêutica devido à sua capacidade de promoverem a sobrevivência, diferenciação, manutenção e proteção dos neurónios contra lesões. O fator neurotrófico derivado de uma linha de células da glia (GDNF) é um potente fator neurotrófico dos neurónios DA da via nigroestriatal. Os aumentos na expressão de GDNF em células de estriado protegem os neurónios DA contra a lesão da via nigroestriatal induzida por toxinas e promovem a recuperação de neurónios lesados, sugerindo que o GDNF endógeno pode ser neuroprotetor. Assim, a estimulação farmacológica da síntese de GDNF endógeno no estriado poderá vir a ser uma potencial escolha no tratamento da DP. O principal objetivo deste trabalho foi avaliar se a libertação de moléculas solúveis em consequência da lesão dopaminérgica é capaz de induzir alterações na expressão de GDNF em células de estriado. Utilizaram-se culturas do mesencéfalo ventral obtidas a partir de ratos recém-nascidos ou embriões expostas a H2O2 ou L-DOPA para recolher os meios condicionados, que posteriormente foram aplicados em culturas de estriado. Avaliou-se a expressão de GDNF ao nível da proteína e do mRNA nas células estriatais por Western blot e PCR em tempo real, respetivamente. A lesão dopaminérgica foi avaliada através da expressão de tirosina hidroxilase (TH), por Western blot, e da contagem do número de células que expressam TH, por microscopia de fluorescência. Verificou-se que os fatores solúveis libertados por culturas mistas do mesencéfalo ventral expostas a 50M de H2O2 ou 200M de L-DOPA induziram um aumento nos níveis de mRNA do GDNF nas células do estriado. Este aumento é desencadeado por mediadores solúveis libertados apenas na presença de neurónios DA, pois não observámos aumentos de GDNF nas células estriatias após exposição aos fatores solúveis libertados apenas por astrócitos do mesencéfalo ventral, previamente incubados com os mesmos agentes oxidantes. Foram testadas concentrações superiores de H2O2 e L-DOPA em culturas embrionárias mistas do mesencéfalo ventral. Foi observada uma diminuição no número de células TH+ nestas culturas quando expostas a 600M de L-DOPA ou 400M de H2O2. Verificámos também que os fatores solúveis libertados após lesão dopaminérgica induziram aumentos de GDNF nas células estriatais. Os resultados obtidos neste trabalho indicam que após lesão dos neurónios DA, as células do mesencéfalo ventral libertam mediadores solúveis que atuam ao nível… Advisors/Committee Members: Fonseca, Carla Sofia Pais, Baltazar, Graça Maria Fernandes.

Subjects/Keywords: Doenças neurodegenarativas - Doenças de Parkinson; GDNF - Factores neurotróficos

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Gama, S. M. (2012). Expressão de GDNF em células estriatais: efeito de fatores solúveis libertados por células do mesencéfalo ventral após lesão dopaminérgica. (Thesis). RCAAP. Retrieved from http://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/2864

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Gama, Susana Martins. “Expressão de GDNF em células estriatais: efeito de fatores solúveis libertados por células do mesencéfalo ventral após lesão dopaminérgica.” 2012. Thesis, RCAAP. Accessed January 18, 2021. http://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/2864.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Gama, Susana Martins. “Expressão de GDNF em células estriatais: efeito de fatores solúveis libertados por células do mesencéfalo ventral após lesão dopaminérgica.” 2012. Web. 18 Jan 2021.

Vancouver:

Gama SM. Expressão de GDNF em células estriatais: efeito de fatores solúveis libertados por células do mesencéfalo ventral após lesão dopaminérgica. [Internet] [Thesis]. RCAAP; 2012. [cited 2021 Jan 18]. Available from: http://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/2864.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Gama SM. Expressão de GDNF em células estriatais: efeito de fatores solúveis libertados por células do mesencéfalo ventral após lesão dopaminérgica. [Thesis]. RCAAP; 2012. Available from: http://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/2864

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

12. Bessa, Agustina Morais. GPER: uma nova estratégia de proteção na lesão dopaminérgica ?.

Degree: 2013, RCAAP

URL: https://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/3217

► Estudos epidemiológicos e estudos em modelos da Doença de Parkinson sustentam a hipótese do estrogénio possuir um papel neuroprotetor na via nigrostriatal. Resultados do nosso… (more)

▼ Estudos epidemiológicos e estudos em modelos da Doença de Parkinson sustentam a hipótese do estrogénio possuir um papel neuroprotetor na via nigrostriatal. Resultados do nosso grupo (Campos et al. 2012) mostram que o estrogénio promove a regulação da expressão de GDNF a qual é requerida para a proteção dos neurónios dopaminérgicos pelo 17-β estradiol. Adicionalmente, também mostramos num modelo da doença de Parkinson que a proteção induzida pelo 17-β estradiol não requer a ativação de recetores intracelulares. Com o presente estudo pretendemos investigar o papel de um recetor de estrogénio associado à membrana, na neuroproteção contra a lesão dopaminérgica induzida pelo MPP+ (in vitro) ou MPTP (in vivo). Os nossos resultados mostraram que o G1, um agonista selectivo do recetor, previne a perda dos neurónios dopaminérgicos induzida pela exposição de culturas celulares do mesencéfalo ao MPP+, e que o G15 (o antagonista selectivo do recetor) inibe a neuroproteção induzida pelo estrogénio. Além disso, observamos que a incubação com G1 foi capaz de promover o aumento da expressão de GDNF em culturas primárias do mesencéfalo, e que a imunodepleção do GDNF impede a proteção induzida pela exposição com G1. Avaliamos também a capacidade do G1 em promover a proteção num modelo MPTP de murganho por análise do número de células positivas para tirosina hidroxilase. Usando testes de comportamento, campo aberto e “grip test”, também avaliámos a capacidade do G1 proteger as funções motoras. Os resultados obtidos indicam que a ativação deste receptor efectivamente protege a via nigrostriatal face à lesão induzida pela toxina dopaminérgica através de um processo que envolve a regulação da expressão de GDNF. Estes resultados, conjuntamente com o facto do recetor ser um receptor de estrogénio que não medeia efeitos nos órgãos reprodutores, sugere que pode ser usado como uma estratégia alvo designada para proteger a lesão dopaminérgica. Advisors/Committee Members: Baltazar, Graça Maria Fernandes.

Subjects/Keywords: Estrogénio - Neuroprotecção; Estradiol; Doença e Parkinson - Estrogénio; GDNF

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Bessa, A. M. (2013). GPER: uma nova estratégia de proteção na lesão dopaminérgica ?. (Thesis). RCAAP. Retrieved from https://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/3217

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Bessa, Agustina Morais. “GPER: uma nova estratégia de proteção na lesão dopaminérgica ?.” 2013. Thesis, RCAAP. Accessed January 18, 2021. https://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/3217.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Bessa, Agustina Morais. “GPER: uma nova estratégia de proteção na lesão dopaminérgica ?.” 2013. Web. 18 Jan 2021.

Vancouver:

Bessa AM. GPER: uma nova estratégia de proteção na lesão dopaminérgica ?. [Internet] [Thesis]. RCAAP; 2013. [cited 2021 Jan 18]. Available from: https://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/3217.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Bessa AM. GPER: uma nova estratégia de proteção na lesão dopaminérgica ?. [Thesis]. RCAAP; 2013. Available from: https://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/3217

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Northeastern University

13. Aly, Amirah Emad-Eldin. An intranasal GDNF gene therapy approach for treating Parkinson's disease.

Degree: PhD, School of Pharmacy, 2017, Northeastern University

URL: http://hdl.handle.net/2047/D20260243

► Parkinson's disease (PD) is a progressive neurodegenerative disorder that results from the loss of the A9 nigrostriatal dopamine neurons. The current therapies available for treating… (more)

▼ Parkinson's disease (PD) is a progressive neurodegenerative disorder that results from the loss of the A9 nigrostriatal dopamine neurons. The current therapies available for treating PD provide symptomatic relief by replacing or mimicking dopamine in the brain, but do not actually prevent or reverse the loss of these dopaminergic neurons. Glial cell-line derived neurotrophic factor (GDNF) has disease-modifying potential in PD due to its ability to promote the survival of dopamine neurons both in vitro and in vivo. GDNF has been shown to be neuroprotective in several animal models of PD. However, its clinical potential has been limited thus far by its inability to cross the blood-brain barrier (BBB) and the need for invasive intracranial delivery. The main objective of this thesis was to develop an approach to non-invasively deliver a continuous source of GDNF to the brain at levels that are neuroprotective in Parkinsons Disease, whilst minimizing systemic exposure. To do so, this project investigated the intranasal delivery of non-viral hGDNF expression plasmids (pGDNF_1b and pUGG) compacted into nanoparticles (NPs). Intranasal delivery allows large therapeutics to circumvent the BBB while avoiding peripheral exposure, while a gene therapy approach would provide a long-term renewable source of GDNF in the brain regions associated with PD. These NPs, developed by Copernicus Therapeutics, Inc., are composed of 10 kDa polyethylene glycol-substituted lysine 30-mers (CK30PEG10k) which unimolecularly compact the plasmid DNA into neutrally charged NPs.; The first goal of this project was to determine if intranasal administration of pGDNF_1b DNA NPs produces a neuroprotective and neurotrophic effect on rat substantia nigra (SN) dopamine neurons. The neuroprotective efficacy of this approach was tested in the rat unilateral 6-hydroxydopamine model of PD. Tyrosine hydroxylase (TH) immunostaining density was used as a marker for dopamine neurons in the SN and their nerve terminals in the striatum. Intranasal administration of pGDNF_1b NPs significantly reduced amphetamine-induced rotational behavior, increased TH staining density in both the SN and the striatum, and increased the number of TH-positive dopamine neurons in the SN. These results collectively demonstrated that pGDNF_1b was neuroprotective in this animal model of PD. The neurotrophic effect of pGDNF_1b was studied in the SN and striatum of healthy/intact rats, as well as in the unlesioned SN of 6-OHDA lesioned rats from the previous study. Intranasal pGDNF_1b NPs did not affect TH staining density in either the SN or the striatum of unlesioned rats, but it resulted in increases in TH staining density in the unlesioned SN of 6-OHDA lesioned rats relative to saline-or pGDNF_1b NP-treated unlesioned animals.; The next goals of this thesis were to examine the regional and cellular transfection and distribution pattern, as well as the time-course of transgene expression in the rat brain after intranasal delivery of pUGG NPs. Intranasal administration of pUGG NPs lead to…

Subjects/Keywords: focused ultrasound; GDNF; gene therapy; intranasal; nanoparticles; Parkinson's disease

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Aly, A. E. (2017). An intranasal GDNF gene therapy approach for treating Parkinson's disease. (Doctoral Dissertation). Northeastern University. Retrieved from http://hdl.handle.net/2047/D20260243

Chicago Manual of Style (16^th Edition):

Aly, Amirah Emad-Eldin. “An intranasal GDNF gene therapy approach for treating Parkinson's disease.” 2017. Doctoral Dissertation, Northeastern University. Accessed January 18, 2021. http://hdl.handle.net/2047/D20260243.

MLA Handbook (7^th Edition):

Aly, Amirah Emad-Eldin. “An intranasal GDNF gene therapy approach for treating Parkinson's disease.” 2017. Web. 18 Jan 2021.

Vancouver:

Aly AE. An intranasal GDNF gene therapy approach for treating Parkinson's disease. [Internet] [Doctoral dissertation]. Northeastern University; 2017. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/2047/D20260243.

Council of Science Editors:

Aly AE. An intranasal GDNF gene therapy approach for treating Parkinson's disease. [Doctoral Dissertation]. Northeastern University; 2017. Available from: http://hdl.handle.net/2047/D20260243

14. Irala, Dolores. Nuevas funciones y mecanismos de acción del factor neurotrófico derivado de células gliales, GDNF; en el desarrollo del sistema nervioso.

Degree: 2016, Universidad de Buenos Aires

URL: http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgrauba&cl=CL1&d=HWA_1394 ; http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgrauba/index/assoc/HWA_1394.dir/1394.PDF

►

GDNF and its co-receptor, GFRa1, play a key role in synaptic maturation during\nnervous system development through ligand-induced cell adhesion molecule mechanism.\nThe aim of this project… (more)

▼

GDNF and its co-receptor, GFRa1, play a key role in synaptic maturation during\nnervous system development through ligand-induced cell adhesion molecule mechanism.\nThe aim of this project was to study the role of GDNF and GFRa1 in postsynaptic\nmaturation and development of hippocampal neuronal circuits. We have shown that\nGDNF/GFRa1 complex regulates dendritic growth and complexity of pyramidal neurons\nboth in vitro and in vivo. Furthermore they promote dendritic spine formation and\npostsynaptic maturation recruiting excitatory postsynaptic proteins such as Homer1 and\nNMDAR1 to the postsynaptic density. GFRa1 deficient mice show a reduction in synapse\ndensity and in different synaptic parameters in vivo regarding wild type mice. Finally, we\nhave identified NCAM-180 as the mediator of the intracellular signaling of GDNF/GFRa1\ncomplex in the postsynaptic membrane, since in the absence of this protein postsynaptic\neffects induced by GDNF and GFRa1 are lost.\nIn this thesis we have identified GDNF, GFRa1 and NCAM-180 as a molecular\ncomplex required for neural circuits development, through the regulation of dendritic tree\ngrowth, synapse formation and postsynaptic maturation.

Fil: Irala, Dolores. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina

GDNF y su co-receptor, GFRa1, cumplen un rol clave en la maduración\npresináptica durante el desarrollo del sistema nervioso a través de un mecanismo de\nadhesión trans-homofílico dependiente de ligando. El objetivo general de este proyecto\nfue estudiar el rol del GDNF y GFRa1 en la maduración postsináptica y el establecimiento\nde circuitos hipocampales. Hemos evidenciado que el complejo GDNF/GFRa1 regula el\ncrecimiento y complejidad dendrítica de neuronas piramidales tanto in vitro como in vivo.\nMás aun promueven la formación de espinas dendríticas y su maduración reclutando\nproteínas claves de las sinapsis excitatorias como Homer1 y NMDAR1 a la densidad\npostsináptica. Animales deficientes para GFRa1 presentan una reducción en la densidad\nde sinapsis in vivo así como en distintos parámetros sinápticos respecto a los animales\nsalvajes. Finalmente, identificamos a NCAM-180 como el mediador de la señalización\nintracelular del complejo GDNF-GFRa1 en la membrana postsináptica, ya que en\nausencia de esta proteína se pierden los efectos postsinápticos inducidos por GDNF y su\nreceptor GFRa1.\nEn este trabajo hemos identificado al sistema GDNF/GFRa1/NCAM-180 como\ncomplejo molecular requerido para el armado de los circuitos neuronales, a través de la\nregulación de procesos de crecimiento dendrítico, desarrollo de espinas y maduración de\nla maquinaria postsináptica.

Advisors/Committee Members: Paratcha, Gustavo, Setton, Patricia, Ledda, Fernanda, Pasquini, Juana, Reines, Analía, Schinder, Alejandro.

Subjects/Keywords: GDNF; GFRa1; NCAM; Desarrollo hipocampal; Dendritogénesis; Espinogénesis; Sinaptogénesis

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Irala, D. (2016). Nuevas funciones y mecanismos de acción del factor neurotrófico derivado de células gliales, GDNF; en el desarrollo del sistema nervioso. (Thesis). Universidad de Buenos Aires. Retrieved from http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgrauba&cl=CL1&d=HWA_1394 ; http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgrauba/index/assoc/HWA_1394.dir/1394.PDF

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Irala, Dolores. “Nuevas funciones y mecanismos de acción del factor neurotrófico derivado de células gliales, GDNF; en el desarrollo del sistema nervioso.” 2016. Thesis, Universidad de Buenos Aires. Accessed January 18, 2021. http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgrauba&cl=CL1&d=HWA_1394 ; http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgrauba/index/assoc/HWA_1394.dir/1394.PDF.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Irala, Dolores. “Nuevas funciones y mecanismos de acción del factor neurotrófico derivado de células gliales, GDNF; en el desarrollo del sistema nervioso.” 2016. Web. 18 Jan 2021.

Vancouver:

Irala D. Nuevas funciones y mecanismos de acción del factor neurotrófico derivado de células gliales, GDNF; en el desarrollo del sistema nervioso. [Internet] [Thesis]. Universidad de Buenos Aires; 2016. [cited 2021 Jan 18]. Available from: http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgrauba&cl=CL1&d=HWA_1394 ; http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgrauba/index/assoc/HWA_1394.dir/1394.PDF.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Irala D. Nuevas funciones y mecanismos de acción del factor neurotrófico derivado de células gliales, GDNF; en el desarrollo del sistema nervioso. [Thesis]. Universidad de Buenos Aires; 2016. Available from: http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgrauba&cl=CL1&d=HWA_1394 ; http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgrauba/index/assoc/HWA_1394.dir/1394.PDF

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Helsinki

15. Pulkkinen, Nita. Endogeeninen GDNF dopamiinijärjestelmän säätelijänä : tutkimusvälineenä amfetamiini.

Degree: Farmaceutiska fakulteten, 2013, University of Helsinki

URL: http://hdl.handle.net/10138/40775

► Amfetamiinia ja sen monia johdannaisia käytetään sekä lääkkeinä että stimuloivina huumausaineina. Amfetamiinin merkittävin vaikutus keskushermostossa on voimakas dopamiinin vapautuminen ulos soluista, mikä johtaa dopaminergisen hermovälityksen… (more)

▼ Amfetamiinia ja sen monia johdannaisia käytetään sekä lääkkeinä että stimuloivina huumausaineina. Amfetamiinin merkittävin vaikutus keskushermostossa on voimakas dopamiinin vapautuminen ulos soluista, mikä johtaa dopaminergisen hermovälityksen tehostumiseen. Amfetamiini vaikuttaa samoin myös noradrenaliinin ja serotoniin vapautumiseen, ja epäsuorasti muihinkin välittäjäainejärjestelmiin. Amfetamiinin tarkka vaikutusmekanismi ei ole edelleenkään täysin selvä, mutta sen tiedetään vaikuttavan moniin solunosiin ja hermovälityksen säätelymekanismeihin. mfetamiini on dopamiinitransportterin (DAT) substraatti, ja toimii sen kilpailevana inhibiittorina vähentäen näin dopamiinin takaisinottoa soluihin. Kulkeuduttuaan soluun amfetamiini saa aikaan muutoksia DAT:n toiminnassa, jolloin dopamiinia alkaakin kulkeutua DAT:n kautta ulos solusta. Amfetamiini on myös vesikulaarisen monoamiinitransportteri-2:n (VMAT2) substraatti ja kykenee vapauttamaan dopamiinia solunsisäisistä varastorakkuloista lisäten vapaan dopamiinin pitoisuutta solussa. Lisäksi amfetamiini estää dopamiinin metaboliaa monoamiinioksidaasin (MAO) kautta, lisää dopamiinin synteesiä sekä uusimpien tutkimusten mukaan lisää dopamiinihermosolujen aktiivisuutta ja dopamiinin eksosytoottista vapautumista. Huumausaineriippuvuus on krooninen sairaus, johon liittyy hermoston plastisia muutoksia. GDNF eli gliasolulinjaperäinen hermokasvutekijä on yksi, erityisesti dopamiinijärjestelmän kannalta tärkeä, plastisuutta säätelevä molekyyli, jolla on toivottu olevan jopa riippuvuudelta suojaavia ominaisuuksia. Tässä erikoistyössä tutkittiin, miten endogeenisen GDNF:n ylituotanto vaikuttaa dopamiinijärjestelmään ja erityisesti, millaisina muutoksina tämä näkyy reagoinnissa huumausaineelle. Tutkimuksessa käytettiin endogeenistä GDNF:ää normaalia enemmän ilmentävää hypermorfista hiirikantaa (GDNFh), ja verrokkeina samojen poikueiden villityypin hiiriä. Kokeissa mitattiin mikrodialyysin avulla, miten striatumin ja accumbens-tumakkeen solunulkoinen dopamiinipitoisuus muuttuu amfetamiinistimulaation seurauksena. Amfetamiini annosteltiin suoraan aivoihin mikrodialyysikoettimen kautta. Mikrodialyysi tehtiin kullekin eläimelle koepäivinä 1 ja 4. Välipäivinä hiirille annosteltiin amfetamiinia intraperitoneaalisesti. Tarkoituksena oli selvittää, muuttuuko aivojen dopamiinivaste toistetun amfetamiinistimulaation seurauksena. Lisäksi erikoistyössä tutkittiin mikrodialyysin avulla kolmen pienmolekyylisen GDNF:ää matkivan yhdisteen biologista aktiivisuutta intakteissa aivoissa. GDNFh-heterotsygooteilla solunulkoinen dopamiinipitoisuus nousi striatumissa ensimmäisenä koepäivänä enemmän kuin villityypin hiirillä, eli ne reagoivat amfetamiinille villityypin hiiriä voimakkaammin. DAT-aktiivisuuden on todettu olevan näillä hypermorfisilla hiirillä normaalia suurempi, jolloin amfetamiini kulkeutuu soluihin tehokkaammin. Lisäksi dopamiinin kudospitoisuus striatumissa on korkeampi kuin villityypin hiirillä, joten suuremmat dopamiinivarastot mahdollistavat runsaamman vapautumisen. Neljäntenä…

Subjects/Keywords: GDNF; amfetamiini; dopamiini; vaikutusmekanismi; mikrodialyysi; riippuvuus; Farmakologi; Pharmacology; Farmakologia

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Pulkkinen, N. (2013). Endogeeninen GDNF dopamiinijärjestelmän säätelijänä : tutkimusvälineenä amfetamiini. (Masters Thesis). University of Helsinki. Retrieved from http://hdl.handle.net/10138/40775

Chicago Manual of Style (16^th Edition):

Pulkkinen, Nita. “Endogeeninen GDNF dopamiinijärjestelmän säätelijänä : tutkimusvälineenä amfetamiini.” 2013. Masters Thesis, University of Helsinki. Accessed January 18, 2021. http://hdl.handle.net/10138/40775.

MLA Handbook (7^th Edition):

Pulkkinen, Nita. “Endogeeninen GDNF dopamiinijärjestelmän säätelijänä : tutkimusvälineenä amfetamiini.” 2013. Web. 18 Jan 2021.

Vancouver:

Pulkkinen N. Endogeeninen GDNF dopamiinijärjestelmän säätelijänä : tutkimusvälineenä amfetamiini. [Internet] [Masters thesis]. University of Helsinki; 2013. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10138/40775.

Council of Science Editors:

Pulkkinen N. Endogeeninen GDNF dopamiinijärjestelmän säätelijänä : tutkimusvälineenä amfetamiini. [Masters Thesis]. University of Helsinki; 2013. Available from: http://hdl.handle.net/10138/40775

Washington University in St. Louis

16. Marquardt, Laura. The Effect of GDNF on Schwann Cells and their Role in Peripheral Nerve Regeneration.

Degree: PhD, Biomedical Engineering, 2014, Washington University in St. Louis

URL: https://openscholarship.wustl.edu/eng_etds/58

► Peripheral nerve damage occurs in 1-3% of all traumatic injuries and results in ~200,000 surgical interventions performed each year. Unfortunately, only 25% of surgical… (more)

▼ Peripheral nerve damage occurs in 1-3% of all traumatic injuries and results in ~200,000 surgical interventions performed each year. Unfortunately, only 25% of surgical patients regain full motor function and less than 3% regain sensation. The gold standard surgical repair method for long gaps is the autologous nerve graft, or autograft; however, significant drawbacks include: donor site morbidity, risk of infection, and increased cost. Acellular nerve allografts (ANAs), nerves harvested from cadaveric donors, have shown promise in improving regeneration. However, as ANAs must undergo a decellularization process to remove immunogenic material, they lack much of the trophic support necessary to encourage regeneration of axons to distal targets. The main source of growth factor support and axonal guidance cues comes from Schwann cells (SCs), the glial cells of the peripheral nervous system. Therefore, SC transplantation and growth factor delivery may improve ANA outcomes. In addition to their role in regeneration, SCs have also been classified into motor or sensory phenotypes based on their association with either motor or sensory axons, which become dysregulated when removed from axonal contact. Understanding these phenotypes may play an important role in targeting motor neuron regeneration and functional motor recovery. Furthermore, the use of glial-cell line derived neurotrophic factor (GDNF), a potent stimulator of axon regeneration, has been shown to affect SC differentiation and drive SCs into native motor or sensory phenotypes. Therefore, in this dissertation, we studied the effect of GDNF on SC phenotype and the resulting interactions with neurons in vitro. In addition, we developed a spatially and temporally controlled GDNF delivery system using lentiviral (LV)-based transduction of SCs in order to improve nerve regeneration in a critical rat sciatic nerve injury model. First, we explored the interaction between phenotypically matched/mismatched SCs and neurons using a microdevice platform. Our results indicate that despite loss of axon contact for a significant period, SCs are capable of promoting neurite growth in a phenotype specific manner. Interestingly, preconditioning of SCs with GDNF can overcome phenotype mismatch. To understand this better, we examined GDNF mRNA and protein levels and found that preconditioning of SCs with exogenous GDNF leads to increased endogenous levels. Next, we studied the mechanism by which GDNF drives SC maturation and differentiation. Through targeted siRNA knockdown, we found that a Fyn-mediated GDNF pathway drives SC maturation and endogenous GDNF production. Furthermore, by disrupting this pathway, we remove any positive effects GDNF has on mismatched SC-neuron cultures. We also found that sustained delivery of GDNF using a heparin-based delivery system (HBDS) is capable of driving SC maturation and differentiation. Finally, we designed a GDNF delivery platform using both the HBDS and LV-transduced SCs expressing GDNF under tetracycline induction. The timing of… Advisors/Committee Members: Shelly E Sakiyama-Elbert, Donald Elbert, Kelly Monk, Kristen Naegle.

Subjects/Keywords: Controlled Delivery; GDNF; Peripheral Nerve Regeneration; Schwann Cells; SC Phenotypes; Engineering

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Marquardt, L. (2014). The Effect of GDNF on Schwann Cells and their Role in Peripheral Nerve Regeneration. (Doctoral Dissertation). Washington University in St. Louis. Retrieved from https://openscholarship.wustl.edu/eng_etds/58

Chicago Manual of Style (16^th Edition):

Marquardt, Laura. “The Effect of GDNF on Schwann Cells and their Role in Peripheral Nerve Regeneration.” 2014. Doctoral Dissertation, Washington University in St. Louis. Accessed January 18, 2021. https://openscholarship.wustl.edu/eng_etds/58.

MLA Handbook (7^th Edition):

Marquardt, Laura. “The Effect of GDNF on Schwann Cells and their Role in Peripheral Nerve Regeneration.” 2014. Web. 18 Jan 2021.

Vancouver:

Marquardt L. The Effect of GDNF on Schwann Cells and their Role in Peripheral Nerve Regeneration. [Internet] [Doctoral dissertation]. Washington University in St. Louis; 2014. [cited 2021 Jan 18]. Available from: https://openscholarship.wustl.edu/eng_etds/58.

Council of Science Editors:

Marquardt L. The Effect of GDNF on Schwann Cells and their Role in Peripheral Nerve Regeneration. [Doctoral Dissertation]. Washington University in St. Louis; 2014. Available from: https://openscholarship.wustl.edu/eng_etds/58

17. CHIN MEIYI. GDNF Receptor Complex in Neuronal Differentiation and Breast Cancer.

Degree: 2014, National University of Singapore

URL: http://scholarbank.nus.edu.sg/handle/10635/53627

Subjects/Keywords: GDNF; GDNF receptor isoforms; Ntera2; MCF7; neuronal differentiation; breast cancer

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

MEIYI, C. (2014). GDNF Receptor Complex in Neuronal Differentiation and Breast Cancer. (Thesis). National University of Singapore. Retrieved from http://scholarbank.nus.edu.sg/handle/10635/53627

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

MEIYI, CHIN. “GDNF Receptor Complex in Neuronal Differentiation and Breast Cancer.” 2014. Thesis, National University of Singapore. Accessed January 18, 2021. http://scholarbank.nus.edu.sg/handle/10635/53627.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

MEIYI, CHIN. “GDNF Receptor Complex in Neuronal Differentiation and Breast Cancer.” 2014. Web. 18 Jan 2021.

Vancouver:

MEIYI C. GDNF Receptor Complex in Neuronal Differentiation and Breast Cancer. [Internet] [Thesis]. National University of Singapore; 2014. [cited 2021 Jan 18]. Available from: http://scholarbank.nus.edu.sg/handle/10635/53627.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

MEIYI C. GDNF Receptor Complex in Neuronal Differentiation and Breast Cancer. [Thesis]. National University of Singapore; 2014. Available from: http://scholarbank.nus.edu.sg/handle/10635/53627

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of California – Berkeley

18. Kolstad, Kathleen Durgin. Development and Assessment of Gene Therapies for.

Degree: Molecular & Cell Biology, 2009, University of California – Berkeley

URL: http://www.escholarship.org/uc/item/1x82h0wb

► Abstract Development and Assessment of Gene Therapies for Inherited Blinding Diseases By Kathleen Durgin Kolstad Doctor of Philosophy in Molecular and Cell Biology University of… (more)

▼ Abstract Development and Assessment of Gene Therapies for Inherited Blinding Diseases By Kathleen Durgin Kolstad Doctor of Philosophy in Molecular and Cell Biology University of California, Berkeley Professor John Flannery, Committee Chair There are two therapeutic approaches for inherited retinal disease addressed in this dissertation: we sought to slow retinal degeneration and reverse visual loss after complete photoreceptor apoptosis. In the first approach, by viral gene transfer to the support cells of the retina, Müller glia (RMCs), we achieved sustained secretion of human glial derived neurotrophic factor (hGDNF) (Chapter 3). We hypothesized that hGDNF production by retinal glia will enhance the protective affects of RMCs in the diseased retina and help slow photoreceptor degeneration. Furthermore, this method avoids extra photoreceptor stress caused by direct hGDNF gene transfer to cells that are already stressed. We were able to optimize gene transfer to RMCs and observe the beginnings of functional rescue in an animal model of autosomal dominant retinitis pigmentosa with this technique. One major advantage of this therapeutic approach is that it is applicable to multiple retinal disease genotypes. The second approach to ocular gene therapy presented in this dissertation was to re-introduce photosensitivity to the retina after complete photoreceptor degeneration (Chapter 4). To this end, we employed the engineered light activated glutamate receptor (LiGluR) to confer light sensitivity on retinal ganglion cells (RGCs) in the diseased retina. We first showed LiGluR mediated RGC photo-activation in in vitro retinal tissue preparation. We then characterized in vivo cell population responses (visually evoked potentials, VEPs) in V1 when retinal input was limited to LiGluR induced activity in the retina. VEPs driven by LiGluR are approximately 50% of the amplitude of full field light flash driven responses in the wild type animal. LiGluR driven cortical responses in blind animals suggest that it is a promising therapy for restoring visual function and processing in the late stages of retinal degeneration. In the third part of this dissertation (Chapter 2a and 2b), the goal was to develop and assess methods of making ocular gene therapies safer and more efficacious. Current gene therapies for retinal degenerative diseases rely on subretinal delivery of viral vectors carrying therapeutic DNA. However, this method of delivery limits the viral transduction profile to the region of injection and seriously compromises the retina during detachment. We have identified natural barriers to viral vector delivery to the outer retina from the vitreous. Furthermore, we have developed artificial methods and characterized disease states that allow these barriers to be overcome. The understanding of and the ability to manipulate barriers to vitreal delivery of viral vectors will help avoid the limitations, risks, and damage associated with subretinal injections.

Subjects/Keywords: Biology, Molecular; Biology, Neuroscience; AAV; GDNF; Gene Therapy; LiGluR; Retina; Retinitis Pigmentosa

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kolstad, K. D. (2009). Development and Assessment of Gene Therapies for. (Thesis). University of California – Berkeley. Retrieved from http://www.escholarship.org/uc/item/1x82h0wb

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Kolstad, Kathleen Durgin. “Development and Assessment of Gene Therapies for.” 2009. Thesis, University of California – Berkeley. Accessed January 18, 2021. http://www.escholarship.org/uc/item/1x82h0wb.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Kolstad, Kathleen Durgin. “Development and Assessment of Gene Therapies for.” 2009. Web. 18 Jan 2021.

Vancouver:

Kolstad KD. Development and Assessment of Gene Therapies for. [Internet] [Thesis]. University of California – Berkeley; 2009. [cited 2021 Jan 18]. Available from: http://www.escholarship.org/uc/item/1x82h0wb.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Kolstad KD. Development and Assessment of Gene Therapies for. [Thesis]. University of California – Berkeley; 2009. Available from: http://www.escholarship.org/uc/item/1x82h0wb

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Queens University

19. Cirella, Kirsten. Inflammation Promotes the Processing of Glial Cell-Line Derived Neurotrophic Factor by Matrix Metalloproteinase-9 in Intestinal Smooth Muscle Cells .

Degree: Neuroscience Studies, 2016, Queens University

URL: http://hdl.handle.net/1974/14052

► The control and regulation of all major intestinal functions are coordinated by neurons within the enteric nervous system (ENS). While intestinal inflammation initially causes a… (more)

▼ The control and regulation of all major intestinal functions are coordinated by neurons within the enteric nervous system (ENS). While intestinal inflammation initially causes a profound loss of enteric neurons, the ENS demonstrates remarkable changes in neuronal structure and function to retain control of gastrointestinal functions. Expression of the neurotrophin glial cell line-derived neurotrophic factor (GDNF) has been implicated in promoting postnatal regenerative processes in the ENS. It has been proposed that intestinal smooth muscle cells (ISMC) express GDNF as a precursor molecule that requires proteolytic processing to achieve the mature form (15 kDa). The expression of mature GDNF is increased during intestinal inflammation, however, little is known about how inflammatory conditions affect the synthesis, processing, and biological activity of GDNF. Analysis of a neonatal rat co-culture model confirmed that the pro-inflammatory cytokine TNF-α caused a 2-fold increase in both the expression of 15 kDa GDNF and in the axonal outgrowth of myenteric neurons, compared to control. Evaluation of broad-spectrum protease inhibitors or inhibitors of metalloproteinases (MMP) showed that only inhibition of MMP-9 specifically blocked TNFα-induced axonal proliferation. The inhibition of MMP-9 in co-cultures also blocked the increase in 15 kDa GDNF expression, while the overall expression of GDNF was not affected. Assessment of MMP-9 expression in ISMC showed that TNF-α caused a greater than 2-fold increase in intracellular expression, compared to control. Significantly, the addition of exogenous 15 kDa GDNF rescued axonal proliferation during MMP-9 inhibition, while transfection with full-length GDNF did not. Finally, a neuron survival bioassay showed that 15 kDa GDNF in conditioned media from a GDNF-expression system doubled enteric neuron survival over serum-free control, while addition of the MMP-9 inhibitor blocked the increase in survival. These findings suggest that both the expression and subsequent intracellular processing of GDNF in the intestine are influenced by inflammatory factors, through the induction of MMP-9 activity. Furthermore, this evidence indicates that GDNF processing to the mature form is required for GDNF-mediated neurotrophic outcomes in the co-culture model.

Subjects/Keywords: Axonal Outgrowth ; TNF-alpha ; GDNF ; Enteric Nervous System ; Intestinal Smooth Muscle Cells ; MMP-9

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Cirella, K. (2016). Inflammation Promotes the Processing of Glial Cell-Line Derived Neurotrophic Factor by Matrix Metalloproteinase-9 in Intestinal Smooth Muscle Cells . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/14052

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Cirella, Kirsten. “Inflammation Promotes the Processing of Glial Cell-Line Derived Neurotrophic Factor by Matrix Metalloproteinase-9 in Intestinal Smooth Muscle Cells .” 2016. Thesis, Queens University. Accessed January 18, 2021. http://hdl.handle.net/1974/14052.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Cirella, Kirsten. “Inflammation Promotes the Processing of Glial Cell-Line Derived Neurotrophic Factor by Matrix Metalloproteinase-9 in Intestinal Smooth Muscle Cells .” 2016. Web. 18 Jan 2021.

Vancouver:

Cirella K. Inflammation Promotes the Processing of Glial Cell-Line Derived Neurotrophic Factor by Matrix Metalloproteinase-9 in Intestinal Smooth Muscle Cells . [Internet] [Thesis]. Queens University; 2016. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1974/14052.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Cirella K. Inflammation Promotes the Processing of Glial Cell-Line Derived Neurotrophic Factor by Matrix Metalloproteinase-9 in Intestinal Smooth Muscle Cells . [Thesis]. Queens University; 2016. Available from: http://hdl.handle.net/1974/14052

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Queens University

20. Han, Tian Yu. Gial cell line-derived neutrotrophic factor expression in proliferating intestinal smooth muscle cells is important for enteric neuron survival .

Degree: Neuroscience Studies, 2012, Queens University

URL: http://hdl.handle.net/1974/7553

► Normal intestinal functions are coordinated by enteric neurons within the enteric nervous system (ENS). In the embryonic and neonatal gut, enteric neuron survival is dependent… (more)

Subjects/Keywords: Enteric nervous system ; ISMC proliferation ; intestinal inflammation ; TNBS-induced colitis ; GDNF ; myenteric plexus ; Enteric neuron

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Han, T. Y. (2012). Gial cell line-derived neutrotrophic factor expression in proliferating intestinal smooth muscle cells is important for enteric neuron survival . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/7553

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Han, Tian Yu. “Gial cell line-derived neutrotrophic factor expression in proliferating intestinal smooth muscle cells is important for enteric neuron survival .” 2012. Thesis, Queens University. Accessed January 18, 2021. http://hdl.handle.net/1974/7553.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Han, Tian Yu. “Gial cell line-derived neutrotrophic factor expression in proliferating intestinal smooth muscle cells is important for enteric neuron survival .” 2012. Web. 18 Jan 2021.

Vancouver:

Han TY. Gial cell line-derived neutrotrophic factor expression in proliferating intestinal smooth muscle cells is important for enteric neuron survival . [Internet] [Thesis]. Queens University; 2012. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1974/7553.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Han TY. Gial cell line-derived neutrotrophic factor expression in proliferating intestinal smooth muscle cells is important for enteric neuron survival . [Thesis]. Queens University; 2012. Available from: http://hdl.handle.net/1974/7553

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Western Michigan University

21. Vianney, John-Mary. Regulation of Glial Cell Line-Derived Neurotrophic Factor (GDNF) Production in Voluntary and Involuntary Muscle.

Degree: PhD, Biological Sciences, 2015, Western Michigan University

URL: https://scholarworks.wmich.edu/dissertations/599

► Glia cell line-derived neurotrophic factor (GDNF) is a survival factor for subpopulations of neurons, including somatic and autonomic motor neurons. These neurons depend, in… (more)

▼ Glia cell line-derived neurotrophic factor (GDNF) is a survival factor for subpopulations of neurons, including somatic and autonomic motor neurons. These neurons depend, in part, on GDNF that is synthesized and secreted by their target tissues. It has been shown that a number of tissues in the periphery express GDNF and these target tissues differ in their composition, function, and in the case of different muscle cell types, their contractile characteristics. Whether the processes regulating GDNF production in these different tissues is similar or different is poorly understood. The broad goal of this study is to examine factors that normally regulate GDNF expression in skeletal and cardiac muscles, with an emphasis on comparing the similarities and differences in these voluntary and involuntary muscles in relation to GDNF production. Previous studies with nervemuscle co-cultures in our laboratory have shown that GDNF protein levels are reduced when skeletal muscle is in contact with cholinergic nerves. Thus, the hypothesis being tested is that cellular activation by neural cells, via neurotransmitter effects, regulates GDNF expression in voluntary and involuntary muscles. Some cultures were electrically stimulated (30min to 48h) to determine whether electrical activity is an important regulator of neurotrophic factor production. Samples of culture medium and cells were collected between 0h and 48h. The results show that acetylcholine inhibits GDNF secretion in both cell types, while electrical stimulation has opposing effects on GDNF production, where GDNF levels increase with long-term electrical stimulation in skeletal muscle and decrease with long-term electrical stimulation in cardiac muscle. When cardiac muscle cells were tested alone, norepinephrine was found to stimulate production of GDNF but inhibit production of nerve growth factor (NGF). Electrical stimulation had a similar effect on NGF and GDNF production in cardiac muscle cells. This work suggests that GDNF expression may be regulated differently in cardiac and skeletal muscle. Understanding the regulation of GDNF production in these tissues will provide a better understanding of how these processes may be modulated therapeutically. Advisors/Committee Members: Dr. John M. Spitsbergen, Dr. Christine Byrd-Jacobs, Dr. Cindy Linn.

Subjects/Keywords: GDNF; Skeletal muscle; Electrical Stimulation; NGF; Cardiac muscle; Neurotransmitters; Biology; Neuroscience and Neurobiology

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Vianney, J. (2015). Regulation of Glial Cell Line-Derived Neurotrophic Factor (GDNF) Production in Voluntary and Involuntary Muscle. (Doctoral Dissertation). Western Michigan University. Retrieved from https://scholarworks.wmich.edu/dissertations/599

Chicago Manual of Style (16^th Edition):

Vianney, John-Mary. “Regulation of Glial Cell Line-Derived Neurotrophic Factor (GDNF) Production in Voluntary and Involuntary Muscle.” 2015. Doctoral Dissertation, Western Michigan University. Accessed January 18, 2021. https://scholarworks.wmich.edu/dissertations/599.

MLA Handbook (7^th Edition):

Vianney, John-Mary. “Regulation of Glial Cell Line-Derived Neurotrophic Factor (GDNF) Production in Voluntary and Involuntary Muscle.” 2015. Web. 18 Jan 2021.

Vancouver:

Vianney J. Regulation of Glial Cell Line-Derived Neurotrophic Factor (GDNF) Production in Voluntary and Involuntary Muscle. [Internet] [Doctoral dissertation]. Western Michigan University; 2015. [cited 2021 Jan 18]. Available from: https://scholarworks.wmich.edu/dissertations/599.

Council of Science Editors:

Vianney J. Regulation of Glial Cell Line-Derived Neurotrophic Factor (GDNF) Production in Voluntary and Involuntary Muscle. [Doctoral Dissertation]. Western Michigan University; 2015. Available from: https://scholarworks.wmich.edu/dissertations/599

Western Michigan University

22. Gyorkos, Amy Morrison. GDNF Content and NMJ Plasticity in Slow and Fast Twitch Myofibers Follows Recruitment in Exercise.

Degree: PhD, Biological Sciences, 2014, Western Michigan University

URL: https://scholarworks.wmich.edu/dissertations/246

► Glial cell-line derived neurotrophic factor (GDNF) supports and maintains the neuromuscular system during development and through adulthood by promoting neuroplasticity. GDNF may play a… (more)

▼ Glial cell-line derived neurotrophic factor (GDNF) supports and maintains the neuromuscular system during development and through adulthood by promoting neuroplasticity. GDNF may play a role in delaying the onset of aging and help compress morbidity by preventing motor unit degeneration. Exercise has been shown to alter GDNF expression differently in slow and fast twitch myofibers. The aim of this dissertation project is to determine if different intensities of exercise can promote changes in GDNF expression and neuromuscular junction (NMJ) morphology in slow and fast twitch muscle fibers. Skeletal muscle fibers were analyzed from adult Sprague Dawley rats aged 4 weeks old and 6 months old. The phenotype of the skeletal myofibers analyzed are from predominantly slow motor units (soleus; SOL) and fast motor units (extensor digitorum longus; EDL and plantaris; PLA). Animals were exercised through voluntary and involuntary means in a swimming barrel and a running wheel with and without resistance for two weeks. The intensity of exercise was altered by different modes of exercise as well as different running speeds and with the use of resistance. GDNF protein content was determined by enzyme-linked immunosorbant assay and immunohistochemistry was utilized to determine myofiber size, end plate measurements, and localization of GDNF. GDNF protein content was increased (P < 0.05) in all recruited myofibers including; slow twitch myofibers (SOL) following all training protocols and fast twitch myofibers (PLA) following higher intensity exercise such as running at speeds faster than 30m/min. Although not significant, GDNF increased 60% in fast twitch EDL myofibers following swim-training. A relationship exists between GDNF protein content and end plate area. These results indicate that GDNF protein content is upregulated in skeletal muscle fibers that are recruited to meet the demands of the given task, in an activity-dependent manner, and induce neuroplasticity at the neuromuscular junction. These findings help to inform exercise prescription to preserve the integrity of the neuromuscular system through aging, injury, and disease. Advisors/Committee Members: Dr. John Spitsbergen, Dr. Christine Byrd-Jacobs, Dr. Christopher Pearl.

Subjects/Keywords: Skeletal muscle; slow twitch; GDNF; fast twitch; neuromuscular junction (NMJ); Rehabilitation and Therapy; Sports Sciences

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Gyorkos, A. M. (2014). GDNF Content and NMJ Plasticity in Slow and Fast Twitch Myofibers Follows Recruitment in Exercise. (Doctoral Dissertation). Western Michigan University. Retrieved from https://scholarworks.wmich.edu/dissertations/246

Chicago Manual of Style (16^th Edition):

Gyorkos, Amy Morrison. “GDNF Content and NMJ Plasticity in Slow and Fast Twitch Myofibers Follows Recruitment in Exercise.” 2014. Doctoral Dissertation, Western Michigan University. Accessed January 18, 2021. https://scholarworks.wmich.edu/dissertations/246.

MLA Handbook (7^th Edition):

Gyorkos, Amy Morrison. “GDNF Content and NMJ Plasticity in Slow and Fast Twitch Myofibers Follows Recruitment in Exercise.” 2014. Web. 18 Jan 2021.

Vancouver:

Gyorkos AM. GDNF Content and NMJ Plasticity in Slow and Fast Twitch Myofibers Follows Recruitment in Exercise. [Internet] [Doctoral dissertation]. Western Michigan University; 2014. [cited 2021 Jan 18]. Available from: https://scholarworks.wmich.edu/dissertations/246.

Council of Science Editors:

Gyorkos AM. GDNF Content and NMJ Plasticity in Slow and Fast Twitch Myofibers Follows Recruitment in Exercise. [Doctoral Dissertation]. Western Michigan University; 2014. Available from: https://scholarworks.wmich.edu/dissertations/246

University of Helsinki

23. Julku, Ulrika. Säädelty geeniterapia Parkinsonin taudin hoidossa.

Degree: Farmaceutiska fakulteten, 2014, University of Helsinki

URL: http://hdl.handle.net/10138/42719

► Parkinsonin tauti on etenevä aivoja rappeuttava sairaus, johon sairastuu noin 1,5-2 % yli 60-vuotiaista. Parkinsonin taudin oireita ovat heikentynyt lihasvoima, lihasjäykkyys, lepovapina ja liikkeiden aloittamisen… (more)

▼ Parkinsonin tauti on etenevä aivoja rappeuttava sairaus, johon sairastuu noin 1,5-2 % yli 60-vuotiaista. Parkinsonin taudin oireita ovat heikentynyt lihasvoima, lihasjäykkyys, lepovapina ja liikkeiden aloittamisen vaikeus. Edetessään tauti voi aiheuttaa motoristen oireiden lisäksi myös psyykkisiä oireita, kuten muistihäiriöitä, ahdistusta ja masennusta. Taudin motoriset oireet johtuvat dopamiinisolujen tuhoutumisesta aivojen nigrostriataalisessa radassa. Nykyisillä lääkkeillä voidaan lievittää Parkinsonin taudin oireita, mutta taudin etenemistä ei voida hidastaa tai pysäyttää. Parkinsonin taudin hoidon kehittämiseksi on tutkittu hermokasvutekijöitä ja geeniterapiaa, joilla on saatu lupaavia tuloksia. Hermokasvutekijät ovat hermosolujen toimintaa sääteleviä proteiineja, joilla on havaittu solujen toimintaa suojaavia ja palauttavia vaikutuksia. Gliasolulinjaperäisellä hermokasvutekijällä (engl. glial cell line -derived neurotrophic factor, GDNF) on saatu lupaavia tuloksia Parkinsonin taudin eläinmalleissa. Kliinisissä kokeissa GDNF-hoidon tulokset ovat kuitenkin olleet vaihtelevia. GDNF hajoaa elimistössä nopeasti, mutta solut voidaan saada pitkäaikaisesti tuottamaan ylimäärin GDNF:ää käyttämällä virusvektoreita, kuten AAV-virusta (engl. adeno-associated virus). GDNF:n kaksi erilaista muotoa, pre-α-pro-GDNF (α-GDNF) ja pre-β-pro-GDNF (β-GDNF), tuotetaan soluissa esiasteina, jotka aktivoidaan proteolyyttisesti. Soluilla tehtyjen kokeiden perusteella nämä kaksi muotoa eroavat erityksensä suhteen. α-muotoa erittyy hermosoluista jatkuvasti ja β-muoto vapautuu hermosoluista fysiologisen stimulaation seurauksena. Aiemmat in vivo -tutkimukset ovat keskittyneet pääosin α-muotoon, mutta β-muoto saattaisi soveltua Parkinsonin taudin hoitoon paremmin kuin α- muoto, koska sen erityksen säätely on fysiologista. Dopamiinisolujen hermokasvutekijä (engl. cerebral dopamine neurotrophic factor, CDNF) on uudempi ja siten vähemmän tutkittu hermokasvutekijä kuin GDNF. Myös CDNF:llä on havaittu dopaminergisiä hermosoluja suojaavia ja palauttavia vaikutuksia Parkinsonin taudin in vivo -malleissa. Tutkimuksen ensimmäisen osan tarkoituksena oli tutkia keskiaivojen mustatumakkeen yläpuolelle annetun CDNF-proteiini-injektion dopamiinihermosoluja palauttavaa vaikutusta rotilla, joiden nigrostriataaliset dopamiinisolut tuhottiin 6-hydroksidopamiini-injektiolla (6-OHDA) mediaaliseen etuaivojuosteeseen (engl. medial forebrain bundle, MFB). Viikko tämän jälkeen rotille annettiin CDNF-, GDNF- tai PBS-injektio. Solutuhon laajuutta ja kehitystä arvioitiin apomorfiinilla (0,1 mg/kg s.c.) ja d-amfetamiinisulfaatilla (2,5 mg/kg s.c.) indusoitujen pyörityskokeiden avulla. Rotat perfusoitiin yhdeksän viikon kuluttua 6-OHDA-injektiosta ja niiden aivoista tehtiin leikkeitä. Tyrosiinihydroksylaasia (TH) sisältävät dopamiinihermosolut värjättiin immunohistokemiallisella menetelmällä. Aivoleikkeistä laskettiin mustatumakkeiden TH-positiiviset solut ja määritettiin TH-positiivisten solujen optinen tiheys aivojuovioissa. Tutkimuksen toisen osan tarkoituksena oli…

Subjects/Keywords: GDNF; 6-OHDA; Parkinsonin tauti; dopamiinisolujen hermokasvutekijä; gliasoluperäinen hermokasvutekijä; Farmakologi; Pharmacology; Farmakologia

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Julku, U. (2014). Säädelty geeniterapia Parkinsonin taudin hoidossa. (Masters Thesis). University of Helsinki. Retrieved from http://hdl.handle.net/10138/42719

Chicago Manual of Style (16^th Edition):

Julku, Ulrika. “Säädelty geeniterapia Parkinsonin taudin hoidossa.” 2014. Masters Thesis, University of Helsinki. Accessed January 18, 2021. http://hdl.handle.net/10138/42719.

MLA Handbook (7^th Edition):

Julku, Ulrika. “Säädelty geeniterapia Parkinsonin taudin hoidossa.” 2014. Web. 18 Jan 2021.

Vancouver:

Julku U. Säädelty geeniterapia Parkinsonin taudin hoidossa. [Internet] [Masters thesis]. University of Helsinki; 2014. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10138/42719.

Council of Science Editors:

Julku U. Säädelty geeniterapia Parkinsonin taudin hoidossa. [Masters Thesis]. University of Helsinki; 2014. Available from: http://hdl.handle.net/10138/42719

University of Helsinki

24. Kontti, Arttu. Tyvitumakkeiden GABAergisen neurotransmission adaptiiviset muutokset Parkinsonin taudissa.

Degree: Farmaceutiska fakulteten, 2014, University of Helsinki

URL: http://hdl.handle.net/10138/144178

► Parkinson's disease causes changes in the basal ganglia GABAergic neurotransmission in addition to the well-known dopaminergic changes. These GABAergic modulations may cause somed of the… (more)

▼ Parkinson's disease causes changes in the basal ganglia GABAergic neurotransmission in addition to the well-known dopaminergic changes. These GABAergic modulations may cause somed of the symptoms not responding well to the standard dopaminergic medication. Neurotrophic factors are a group of endogenous proteins showing promise as a future treatment for Parkinson's disease. They are known to have neuroprotective and neurorestorative effects on the dopaminergic cells. Their effects to the GABAergic cells are still mostly unknown. Intrastriatal injection of GDNF to rats caused significantly slower weight gain compared to CDNF, MANF one week after stereotaxic operation (p=0,002 for CDNF vs. GDNF and p<0,001 for MANF vs. GDNF). Difference to the vehicle (phosphate buffered saline) used as a negative control was not statistically significant (p=0,055). Three weeks after the operation the differences between the treatment groups were no longer statistically significant. Because of problems with the separation in analysis, microdialysis samples remain still to be analysed. To help the analysis of GABA in the future we determined the analytical parameters of the analytical apparatus. We also defined differences in probe permeability between 1 mm and 2 mm probes and between old and new batches. GABA analysis was performed with a HPLC-fluorometric detection of o-phtaldialdehyde-derived GABA. Detection limit for old apparatus was 7,2 nM and for new apparatus 6,2 nM in a sample of 15 µl (0,11 pmol and 93 fmol respectively). Quantification limits defined were 22 nM and 19 nM (0,33 pmol and 0,28 pmol) for the old and the new apparatus, respectively. Upper limit of quantification was estimated to be 246 nM (3,7 pmol). Probes had significant differences in permeability between 1 mm and 2 mm probes, as well as between batches. The variance of permeability of 1 mm probes was estimated to be approximately twofold compared to the 2 mm probes. Furthermore the permeability of 1 mm probes varied between batches significantly. An average of permeability of the old batch was 34 % lower than that of a new batch (p<0,001).

Subjects/Keywords: GDNF; CDNF; MANF; GABA; Parkinson's disease; Basal ganglia; Neurotrophic factors; Microdialysis; HPLC; Farmakologi; Pharmacology; Farmakologia

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kontti, A. (2014). Tyvitumakkeiden GABAergisen neurotransmission adaptiiviset muutokset Parkinsonin taudissa. (Masters Thesis). University of Helsinki. Retrieved from http://hdl.handle.net/10138/144178

Chicago Manual of Style (16^th Edition):

Kontti, Arttu. “Tyvitumakkeiden GABAergisen neurotransmission adaptiiviset muutokset Parkinsonin taudissa.” 2014. Masters Thesis, University of Helsinki. Accessed January 18, 2021. http://hdl.handle.net/10138/144178.

MLA Handbook (7^th Edition):

Kontti, Arttu. “Tyvitumakkeiden GABAergisen neurotransmission adaptiiviset muutokset Parkinsonin taudissa.” 2014. Web. 18 Jan 2021.

Vancouver:

Kontti A. Tyvitumakkeiden GABAergisen neurotransmission adaptiiviset muutokset Parkinsonin taudissa. [Internet] [Masters thesis]. University of Helsinki; 2014. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10138/144178.

Council of Science Editors:

Kontti A. Tyvitumakkeiden GABAergisen neurotransmission adaptiiviset muutokset Parkinsonin taudissa. [Masters Thesis]. University of Helsinki; 2014. Available from: http://hdl.handle.net/10138/144178

25. ZHOU LIHAN. Molecular and cellular functions of the alternatively spliced isoforms of GDNF receptor complex in neuronal differentiation.

Degree: 2012, National University of Singapore

URL: http://scholarbank.nus.edu.sg/handle/10635/35877

Subjects/Keywords: GDNF; GFRa; receptor; isoforms; neuronal; differentiation

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

LIHAN, Z. (2012). Molecular and cellular functions of the alternatively spliced isoforms of GDNF receptor complex in neuronal differentiation. (Thesis). National University of Singapore. Retrieved from http://scholarbank.nus.edu.sg/handle/10635/35877

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

LIHAN, ZHOU. “Molecular and cellular functions of the alternatively spliced isoforms of GDNF receptor complex in neuronal differentiation.” 2012. Thesis, National University of Singapore. Accessed January 18, 2021. http://scholarbank.nus.edu.sg/handle/10635/35877.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

LIHAN, ZHOU. “Molecular and cellular functions of the alternatively spliced isoforms of GDNF receptor complex in neuronal differentiation.” 2012. Web. 18 Jan 2021.

Vancouver:

LIHAN Z. Molecular and cellular functions of the alternatively spliced isoforms of GDNF receptor complex in neuronal differentiation. [Internet] [Thesis]. National University of Singapore; 2012. [cited 2021 Jan 18]. Available from: http://scholarbank.nus.edu.sg/handle/10635/35877.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

LIHAN Z. Molecular and cellular functions of the alternatively spliced isoforms of GDNF receptor complex in neuronal differentiation. [Thesis]. National University of Singapore; 2012. Available from: http://scholarbank.nus.edu.sg/handle/10635/35877

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

26. Shi, Jhih-Yin. Glial Cell LineâDerived Neurotrophic Factor Gene Transfer Exerts Protective Effect on Axons in Sciatic Nerve Following Constriction-Induced Peripheral Nerve Injury.

Degree: PhD, Biological Sciences, 2011, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823111-140424

► Damage to peripheral nerves following trauma or disease has a number of consequences including burning pain, muscle wasting, paralysis, or organ dysfunction. The most common… (more)

▼ Damage to peripheral nerves following trauma or disease has a number of consequences including burning pain, muscle wasting, paralysis, or organ dysfunction. The most common form of neuropathy is that associated with metabolic abnormality, notably diabetes. Many diabetics, especially those with poor blood sugar control, ultimately develop a distal symmetrical and painful neuropathy that initially affects the longest peripheral axons, but with time spreads proximally. Deficiency in neurotrophic support has been proposed to contribute to the development of diabetic neuropathy. Recently, peripheral gene delivery of vascular endothelial growth factor (VEGF), neurotrophin-3 (NT-3), NGF, BDNF or hepatocyte growth factor (HGF) has been shown to facilitate the continuous production of neurotrophic factors and alleviate the diabetic neuropathy. The role of glial cell-derived neurotrophic factor (GDNF) in the pathogenesis and therapeutics of diabetic neuropathy is not well defined. The main objectives of this research sought to inspect the protective effect of GDNF peripheral gene delivery during hyperglycemia- or constriction- induced sciatic nerve injury in rats. In present proposal, we propose to investigate the change in organization and expressions of GDNF signaling complex in the sciatic nerve following injury in the initial stage. Subsequently, the recombinant adenovirus was used gene delivery system for GDNF to evaluate the potential of intramuscular administration of gene delivery for prevent nerve degeneration, and the molecular mechanism of GDNF to ameliorate neuropathy will be clarified. The above study would enable us to test the hypothesis that the topical gene delivery might be a suitable strategy for the treatment of diabetic neuropathy and other disorders in peripheral nerve. Furthermore, the results of animal studies might be extrapolated for future clinical application. Advisors/Committee Members: Huang, Hung-Tu (chair), Chao, David (committee member), Chen, Lee-Wei (chair), Cheng, Jiin-Tsuey (chair), Tai, ming-hong (committee member), Hsu, Ching-Mei (chair).

Subjects/Keywords: Angiogenesis; Diabetes; Diabetic neuropathy; GDNF; Gene delivery

…derived neurotrophic factor (GDNF) in the pathogenesis of diabetic neuropathy remains… …unclear. The present study evaluated the pathogenic role of GDNF deficiency and the therapeutic… …potential of GDNF gene transfer for diabetic neuropathy. After injection of streptozotocin (… …GDNF/GFR1/Akt signaling cascade and depletion of sensory neuropeptides in the peripheral… …nerves. After detection of neuropathy, intramuscular GDNF gene transfer reversed the deficiency…

10 more images…

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Shi, J. (2011). Glial Cell LineâDerived Neurotrophic Factor Gene Transfer Exerts Protective Effect on Axons in Sciatic Nerve Following Constriction-Induced Peripheral Nerve Injury. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823111-140424

Chicago Manual of Style (16^th Edition):

Shi, Jhih-Yin. “Glial Cell LineâDerived Neurotrophic Factor Gene Transfer Exerts Protective Effect on Axons in Sciatic Nerve Following Constriction-Induced Peripheral Nerve Injury.” 2011. Doctoral Dissertation, NSYSU. Accessed January 18, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823111-140424.

MLA Handbook (7^th Edition):

Shi, Jhih-Yin. “Glial Cell LineâDerived Neurotrophic Factor Gene Transfer Exerts Protective Effect on Axons in Sciatic Nerve Following Constriction-Induced Peripheral Nerve Injury.” 2011. Web. 18 Jan 2021.

Vancouver:

Shi J. Glial Cell LineâDerived Neurotrophic Factor Gene Transfer Exerts Protective Effect on Axons in Sciatic Nerve Following Constriction-Induced Peripheral Nerve Injury. [Internet] [Doctoral dissertation]. NSYSU; 2011. [cited 2021 Jan 18]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823111-140424.

Council of Science Editors:

Shi J. Glial Cell LineâDerived Neurotrophic Factor Gene Transfer Exerts Protective Effect on Axons in Sciatic Nerve Following Constriction-Induced Peripheral Nerve Injury. [Doctoral Dissertation]. NSYSU; 2011. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823111-140424

Universidade do Rio Grande do Sul

27. Rosa, Adriane Ribeiro. Marcadores biológicos e nível de funcionalidade em pacientes bipolares.

Degree: 2007, Universidade do Rio Grande do Sul

URL: http://hdl.handle.net/10183/10328

►

Alterações em estruturas específicas do SNC, em particular, no sistema fronto-límbico, assim como a diminuição das células neuronais e gliais parece estar envolvida com a… (more)

▼

Alterações em estruturas específicas do SNC, em particular, no sistema fronto-límbico, assim como a diminuição das células neuronais e gliais parece estar envolvida com a fisiopatologia do Transtorno do Humor Bipolar (THB). A glia exerce um importante papel no SNC, entre os quais, a produção de neurotrofinas, em especial, o Fator de Crescimento Neurotrófico derivado de Células da Glia (GDNF). Um marcado aumento dos níveis séricos de GDNF em pacientes deprimidos (F= 42.31; p=0.004; one-way ANOVA) e maníacos (F= 42.31; p=0.001; one-way ANOVA) foi demonstrado neste estudo, sugerindo um possível envolvimento desta neurotrofina com o THB. Por outro lado, alterações nos fatores neurotróficos afetam os mecanismos de plasticidade sináptica, podendo contribuir para as deficiências cognitivas apresentadas pelos pacientes. Deficiências cognitivas, em especial, as falhas de memória são descritas, as quais influenciam a funcionalidade destes indivíduos, principalmente a nível ocupacional e social. As altas taxas de disfuncionalidade apresentadas pelos pacientes e a falta de padronização dos instrumentos usados nos estudos para avaliar funcionalidade, nos levaram ao desenvolvimento de uma escala. A Escala Breve de Funcionalidade (FAST) é um instrumento de rápida e fácil aplicação desenvolvida para usar em psiquiatria, em especial, paciente com THB. A FAST avalia objetivamente seis áreas específicas da funcionalidade, tais como autonomia, trabalho, cognição, relacionamentos interpessoais, finanças e lazer. A validação da escala foi realizada através de testes psicométricos, tais como: consistência interna (alfa de Cronbach’s igual a 0.909), validade concorrente comparada com a GAF (r=-0.903; p<0.001), test-retest (0.98; p<0.01), validade em detectar diferenças entre episódios agudos (maníacos: 40.44±9.15 e deprimidos 43.21±13.34) e períodos de remissão (18.55±13.19; F=35.43; p<0.001) e análise fatorial. Os resultados obtidos foram muito positivos, tornando o instrumento válido e prontamente disponível para o uso na prática clínica e investigação. Palavras-chave: transtorno do humor bipolar, GDNF, glia, neurotrofinas, funcionalidade, disfuncionalidade, escalas de funcionalidade.

Alterations in specific structures of CNS, in particular, fronto-lymbic system, and a reduction of neurons and glial cells appear to be involved in the pathophysiology of bipolar disorder. Glial cells have an important role in the CNS, for example, the production of neurotrophins, especially, Glial Cell Line-derived Neurotrophic Factor (GDNF). In this study, we showed a marked increased in the serum levels of GDNF in depressive (F= 42.31; p=0.004; one-way ANOVA) and manic bipolar patients (F= 42.31; p=0.001; one-way ANOVA), which suggested that GDNF could be involved in the physiopathology of bipolar disorder. On the other hand, alterations in the neurotrophic factors hinder synaptic plasticity mechanisms, may result in cognitive impairment in bipolar patients. In particular, memory difficulties have been reported here, and these difficulties influence…

Advisors/Committee Members: Kapczinski, Flávio Pereira.

Subjects/Keywords: Transtorno bipolar; Bipolar disorder; Sistema nervoso central; GDNF; Glia; Fatores de crescimento neural; Neuroglia; Neurotophins; Functioning; Impairment functional; Functioning scale

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Rosa, A. R. (2007). Marcadores biológicos e nível de funcionalidade em pacientes bipolares. (Thesis). Universidade do Rio Grande do Sul. Retrieved from http://hdl.handle.net/10183/10328

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Rosa, Adriane Ribeiro. “Marcadores biológicos e nível de funcionalidade em pacientes bipolares.” 2007. Thesis, Universidade do Rio Grande do Sul. Accessed January 18, 2021. http://hdl.handle.net/10183/10328.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Rosa, Adriane Ribeiro. “Marcadores biológicos e nível de funcionalidade em pacientes bipolares.” 2007. Web. 18 Jan 2021.

Vancouver:

Rosa AR. Marcadores biológicos e nível de funcionalidade em pacientes bipolares. [Internet] [Thesis]. Universidade do Rio Grande do Sul; 2007. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10183/10328.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Rosa AR. Marcadores biológicos e nível de funcionalidade em pacientes bipolares. [Thesis]. Universidade do Rio Grande do Sul; 2007. Available from: http://hdl.handle.net/10183/10328

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Kyoto University / 京都大学

28. Mahesh, Gajanan Sahare. Establishment of Long-Term Culture and Elucidation of Self-Renewal Mechanisms of Primitive Male Germ Cells in Cattle : ウシ雄性生殖幹細胞の長期培養系の確立と細胞増殖メカニズムの解明に関する研究.

Degree: 博士(農学), 2015, Kyoto University / 京都大学

URL: http://hdl.handle.net/2433/200509 ; http://dx.doi.org/10.14989/doctor.k19243

新制・課程博士

甲第19243号

農博第2140号

Subjects/Keywords: GDNF; gonocytes; self-renewal; KSR; long-term-culture; testis

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mahesh, G. S. (2015). Establishment of Long-Term Culture and Elucidation of Self-Renewal Mechanisms of Primitive Male Germ Cells in Cattle : ウシ雄性生殖幹細胞の長期培養系の確立と細胞増殖メカニズムの解明に関する研究. (Thesis). Kyoto University / 京都大学. Retrieved from http://hdl.handle.net/2433/200509 ; http://dx.doi.org/10.14989/doctor.k19243

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Mahesh, Gajanan Sahare. “Establishment of Long-Term Culture and Elucidation of Self-Renewal Mechanisms of Primitive Male Germ Cells in Cattle : ウシ雄性生殖幹細胞の長期培養系の確立と細胞増殖メカニズムの解明に関する研究.” 2015. Thesis, Kyoto University / 京都大学. Accessed January 18, 2021. http://hdl.handle.net/2433/200509 ; http://dx.doi.org/10.14989/doctor.k19243.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Mahesh, Gajanan Sahare. “Establishment of Long-Term Culture and Elucidation of Self-Renewal Mechanisms of Primitive Male Germ Cells in Cattle : ウシ雄性生殖幹細胞の長期培養系の確立と細胞増殖メカニズムの解明に関する研究.” 2015. Web. 18 Jan 2021.

Vancouver:

Mahesh GS. Establishment of Long-Term Culture and Elucidation of Self-Renewal Mechanisms of Primitive Male Germ Cells in Cattle : ウシ雄性生殖幹細胞の長期培養系の確立と細胞増殖メカニズムの解明に関する研究. [Internet] [Thesis]. Kyoto University / 京都大学; 2015. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/2433/200509 ; http://dx.doi.org/10.14989/doctor.k19243.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Mahesh GS. Establishment of Long-Term Culture and Elucidation of Self-Renewal Mechanisms of Primitive Male Germ Cells in Cattle : ウシ雄性生殖幹細胞の長期培養系の確立と細胞増殖メカニズムの解明に関する研究. [Thesis]. Kyoto University / 京都大学; 2015. Available from: http://hdl.handle.net/2433/200509 ; http://dx.doi.org/10.14989/doctor.k19243

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

29. Tomé, Diogo Alexandre da Silva. Modulation of Microglial Activity by GDNF.

Degree: 2015, RCAAP

URL: https://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/5963

►

Parkinson’s disease (PD) is an age-related disease characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Increasing evidence suggests that… (more)

▼

Parkinson’s disease (PD) is an age-related disease characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Increasing evidence suggests that inflammation and oxidative stress mediated by activated microglia, the resident immune cells of the central nervous system (CNS), play a critical role in dopaminergic neuronal loss and in the pathophysiology of PD. For this reason, it is crucial to understand the mechanisms capable of controlling microglial reactivity. Glial cell line-derived neurotrophic factor (GDNF), a potent neuroprotective factor for dopaminergic neurons, is able to inhibit the increase in the production of reactive oxygen species (ROS) and in the phagocytosis triggered by an inflammatory agent in midbrain microglial cells, but the mechanisms by which GDNF exerts its effects on microglia are still not completely understood. The control of microglia activation exerted by GDNF depends on GFRa1. However, the signalling mechanism mediated by this co-receptor can be coupled to the transmembrane RET tyrosine kinase or to the cell adhesion molecule NCAM. To elucidate which are the signalling pathways involved in the modulation of microglial activity by GDNF, the effect of GDNF on the activity of RET and of the NCAM target, the focal adhesion kinase (FAK), and the effect of FAK inhibition in GDNF action were evaluated. For these experiments, LPS-stimulated midbrain microglia cultures were used. GDNF was able to inhibit the increase in the number of phagocytic cells triggered by LPS in midbrain microglia cultures when FAK was inhibited. Furthermore, GDNF had no effect on FAK phosphorylation levels but it seems to prevent the decrease in RET phosphorylation levels induced by LPS. In order to determine possible changes in GDNF levels, or in the proteins associated with GDNF signal transduction in PD, an animal model of PD based on the intranigral injection of LPS was used. The results showed that exposure to LPS induces a significant reduction in the GFRa-1 levels in the injected SN. Taken together, these results suggest that the modulation of microglial activity by GDNF involves the receptor RET and not the cell adhesion molecule NCAM. Furthermore, the GDNF signalling may be impaired in PD due to low levels of GDNF co-receptor GFRa-1 in the SN of LPS-exposed animals.

A doença de Parkinson é a segunda doença neurodegenerativa mais comum depois da doença de Alzheimer. É uma doença associada ao envelhecimento que afecta cerca de 0,3% da população nos países desenvolvidos. A sua principal característica patológica é a perda dos neurónios dopaminérgicos da substantia nigra pars compacta, ao nível do mesencéfalo, o que resulta numa diminuição de dopamina no estriado. Esta diminuição traduz-se principalmente em sintomas motores como tremor, bradicinesia, rigidez muscular e instabilidade postural. No entanto, sintomas não motores como depressão, distúrbios no sono, alterações sensoriais e cognitivas são também característicos desta patologia. Apesar de a sua etiologia não…

Advisors/Committee Members: Baltazar, Graça Maria Fernandes, Oliveira, Julieta.

Subjects/Keywords: Doença de Parkinson; Gdnf; Gfra1; Microglia; Ncam; Neuroinflamação; Ret; Stress Oxidativo; Domínio/Área Científica::Ciências Médicas::Ciências da Saúde

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Tomé, D. A. d. S. (2015). Modulation of Microglial Activity by GDNF. (Thesis). RCAAP. Retrieved from https://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/5963

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Tomé, Diogo Alexandre da Silva. “Modulation of Microglial Activity by GDNF.” 2015. Thesis, RCAAP. Accessed January 18, 2021. https://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/5963.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Tomé, Diogo Alexandre da Silva. “Modulation of Microglial Activity by GDNF.” 2015. Web. 18 Jan 2021.

Vancouver:

Tomé DAdS. Modulation of Microglial Activity by GDNF. [Internet] [Thesis]. RCAAP; 2015. [cited 2021 Jan 18]. Available from: https://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/5963.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Tomé DAdS. Modulation of Microglial Activity by GDNF. [Thesis]. RCAAP; 2015. Available from: https://www.rcaap.pt/detail.jsp?id=oai:ubibliorum.ubi.pt:10400.6/5963

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Wayne State University

30. Broadrick, Kristy. Characterizing The Controlled Release Of Glial Cell-Line Derived (gdnf) Neurotrophic Factor From Encapsulated Schwann Cells.

Degree: MS, Biomedical Engineering, 2010, Wayne State University

URL: https://digitalcommons.wayne.edu/oa_theses/18

► ABSTRACT CHARACTERIZING THE CONTROLLED RELEASE OF GDNF IN SCHWANN CELLS by KRISTY BROADRICK May 2010 Advisor: Dr. Pamela VandeVord Major: Biomedical Engineering Degree: Masters… (more)

Subjects/Keywords: Alginate; Glial cell line derived neurotrophic factor (GDNF); inducible expression; Microencapsulation; Ponasterone A; Schwann cell; Biomedical Engineering and Bioengineering

Record Details Similar Records Cite « Share

❌

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Broadrick, K. (2010). Characterizing The Controlled Release Of Glial Cell-Line Derived (gdnf) Neurotrophic Factor From Encapsulated Schwann Cells. (Masters Thesis). Wayne State University. Retrieved from https://digitalcommons.wayne.edu/oa_theses/18

Chicago Manual of Style (16^th Edition):

Broadrick, Kristy. “Characterizing The Controlled Release Of Glial Cell-Line Derived (gdnf) Neurotrophic Factor From Encapsulated Schwann Cells.” 2010. Masters Thesis, Wayne State University. Accessed January 18, 2021. https://digitalcommons.wayne.edu/oa_theses/18.

MLA Handbook (7^th Edition):

Broadrick, Kristy. “Characterizing The Controlled Release Of Glial Cell-Line Derived (gdnf) Neurotrophic Factor From Encapsulated Schwann Cells.” 2010. Web. 18 Jan 2021.

Vancouver:

Broadrick K. Characterizing The Controlled Release Of Glial Cell-Line Derived (gdnf) Neurotrophic Factor From Encapsulated Schwann Cells. [Internet] [Masters thesis]. Wayne State University; 2010. [cited 2021 Jan 18]. Available from: https://digitalcommons.wayne.edu/oa_theses/18.

Council of Science Editors:

Broadrick K. Characterizing The Controlled Release Of Glial Cell-Line Derived (gdnf) Neurotrophic Factor From Encapsulated Schwann Cells. [Masters Thesis]. Wayne State University; 2010. Available from: https://digitalcommons.wayne.edu/oa_theses/18

		in
And / Or
		in
And / Or
		in
And / Or
		in

Open Access Theses and Dissertations