subject:(T type calcium channel)

University of Sydney

1. Perera, Naomi Tessa. ZnT‐1 expression in the preimplantation mouse embryo and its effect on calcium influx .

Degree: 2014, University of Sydney

► ZnT-1 expression in the pre-implantation mouse embryo and its effect on calcium influx Pre-implantation embryos develop into 9 stages over the first 5 days post-fertilisation.… (more)

Subjects/Keywords: preimplantation; mouse; embryo; ZnT-1; L-type; T-type; calcium channel

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APA (6^th Edition):

Perera, N. T. (2014). ZnT‐1 expression in the preimplantation mouse embryo and its effect on calcium influx . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/13519

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):

Perera, Naomi Tessa. “ZnT‐1 expression in the preimplantation mouse embryo and its effect on calcium influx .” 2014. Thesis, University of Sydney. Accessed April 18, 2021. http://hdl.handle.net/2123/13519.

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

MLA Handbook (7^th Edition):

Perera, Naomi Tessa. “ZnT‐1 expression in the preimplantation mouse embryo and its effect on calcium influx .” 2014. Web. 18 Apr 2021.

Vancouver:

Perera NT. ZnT‐1 expression in the preimplantation mouse embryo and its effect on calcium influx . [Internet] [Thesis]. University of Sydney; 2014. [cited 2021 Apr 18]. Available from: http://hdl.handle.net/2123/13519.

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

Council of Science Editors:

Perera NT. ZnT‐1 expression in the preimplantation mouse embryo and its effect on calcium influx . [Thesis]. University of Sydney; 2014. Available from: http://hdl.handle.net/2123/13519

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

Loyola University Chicago

2. Keeling, Ginny Marie. Determination of the Molecular Mechanisms of Hyperglycemia-Induced Changes in Cav3.2 Calcium Channel Properties.

Degree: MS, Neuroscience, 2012, Loyola University Chicago

URL: https://ecommons.luc.edu/luc_theses/841

► Hyperglycemia can cause altered excitability due to increased CaV3.2 T-type calcium channel function, bestowing diabetics an increased neuropathy risk. The objective of this study… (more)

Subjects/Keywords: calcium channel; diabetes; ganglioside; glycosylation; T-type; Neurosciences

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APA (6^th Edition):

Keeling, G. M. (2012). Determination of the Molecular Mechanisms of Hyperglycemia-Induced Changes in Cav3.2 Calcium Channel Properties. (Thesis). Loyola University Chicago. Retrieved from https://ecommons.luc.edu/luc_theses/841

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):

Keeling, Ginny Marie. “Determination of the Molecular Mechanisms of Hyperglycemia-Induced Changes in Cav3.2 Calcium Channel Properties.” 2012. Thesis, Loyola University Chicago. Accessed April 18, 2021. https://ecommons.luc.edu/luc_theses/841.

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

MLA Handbook (7^th Edition):

Keeling, Ginny Marie. “Determination of the Molecular Mechanisms of Hyperglycemia-Induced Changes in Cav3.2 Calcium Channel Properties.” 2012. Web. 18 Apr 2021.

Vancouver:

Keeling GM. Determination of the Molecular Mechanisms of Hyperglycemia-Induced Changes in Cav3.2 Calcium Channel Properties. [Internet] [Thesis]. Loyola University Chicago; 2012. [cited 2021 Apr 18]. Available from: https://ecommons.luc.edu/luc_theses/841.

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

Council of Science Editors:

Keeling GM. Determination of the Molecular Mechanisms of Hyperglycemia-Induced Changes in Cav3.2 Calcium Channel Properties. [Thesis]. Loyola University Chicago; 2012. Available from: https://ecommons.luc.edu/luc_theses/841

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

Temple University

3. Wang, Fang. DOES CALCIUM INFLUX THROUGH T-TYPE CALCIUM CHANNEL INDUCE CARDIOMYOCYTE PROLIFERATION?.

Degree: PhD, 2012, Temple University

URL: http://digital.library.temple.edu/u?/p245801coll10,214814

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Physiology

Cardiovascular disease remains the number one cause or mortally in the western world. Heart failure is the most rapidly growing cardiovascular disease (Hobbs, 2004;… (more)

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Physiology

Cardiovascular disease remains the number one cause or mortally in the western world. Heart failure is the most rapidly growing cardiovascular disease (Hobbs, 2004; Levy, et al., 2002). Heart failure, by definition, is progressive deteriorating function of the heart due to progressive cardiac myocytes loss. Though after decades of endeavor of searching the pathophysiology and treatments for heart failure, it remains highly lethal. Therefore, it is vital to find novel therapies to help treat such chronic disease. Replace the lost cardiomyocyte with new ones could restore cardiac function and reduce mortality. The purpose of this study is to investigate on how TTCCs (T-type calcium channels) affect cardiomyocyte proliferation. In mice after birth, the major TTCC expressed in the heart is Cav3.1/α1G, and therefore we used Cav3.1/α1G transgenic (TG), knockout (-/-) and wild type mice respectively to define the role of TTCC in cardiomyocyte proliferation. In neonatal mouse ventricular myocyte (NMVMs) right after birth, there is almost no TTCC after birth in α1G-/- NMVMs, whereas there are around 35% NMVMs in wild type (WT) show TTCC. On day 7 after birth, there are no T-type calcium currents in both α1G-/- NMVMs and WT NMVMs. Using BrdU, a DNA synthesis marker, we identified plenty of BrdU positive cardiomyocyte during the first seven days after birth. Cardiomyocyte is special due to its double nucleation property. Our cell cycle studies showed that there is significant difference in cell cycle distribution between α1G-/- and WT NMVMs on day seven after birth. Significantly more NMVMs are arrested in G1 phase in α1G-/-, compared to WT NMVMs. Even until 2 month old, there are still significantly more mono-nucleated cardiomyocyte in α1G-/- than in WT. In conclusion, all these evidence showed that blocking T-type calcium channel could partially prevent binucleation from happening and stop cardiomyocytes withdrawal from cell cycle. Mononucleated cardiomyocyte is still able to proliferate. Hence, mononucleated cardiomyocytes in adult still have potential to proliferation because these cardiomyoctes are arrested in their cell-cycle before their terminal differentiation, which could offer a novel approach for cardiac repair.

Temple University – Theses

Advisors/Committee Members: Houser, Steven R., Chen, Xiongwen, Scalia, Rosario, Sabri, Abdelkarim, Wang, Hong.

Subjects/Keywords: Physiology; Calcium Current; Cardiomyocyte Proliferation; Electrophysiology; Flow Cytometry; Neonatal Mice Ventricular Cardiomyocyte; T-type calcium channel

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

APA (6^th Edition):

Wang, F. (2012). DOES CALCIUM INFLUX THROUGH T-TYPE CALCIUM CHANNEL INDUCE CARDIOMYOCYTE PROLIFERATION?. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,214814

Chicago Manual of Style (16^th Edition):

Wang, Fang. “DOES CALCIUM INFLUX THROUGH T-TYPE CALCIUM CHANNEL INDUCE CARDIOMYOCYTE PROLIFERATION?.” 2012. Doctoral Dissertation, Temple University. Accessed April 18, 2021. http://digital.library.temple.edu/u?/p245801coll10,214814.

MLA Handbook (7^th Edition):

Wang, Fang. “DOES CALCIUM INFLUX THROUGH T-TYPE CALCIUM CHANNEL INDUCE CARDIOMYOCYTE PROLIFERATION?.” 2012. Web. 18 Apr 2021.

Vancouver:

Wang F. DOES CALCIUM INFLUX THROUGH T-TYPE CALCIUM CHANNEL INDUCE CARDIOMYOCYTE PROLIFERATION?. [Internet] [Doctoral dissertation]. Temple University; 2012. [cited 2021 Apr 18]. Available from: http://digital.library.temple.edu/u?/p245801coll10,214814.

Council of Science Editors:

Wang F. DOES CALCIUM INFLUX THROUGH T-TYPE CALCIUM CHANNEL INDUCE CARDIOMYOCYTE PROLIFERATION?. [Doctoral Dissertation]. Temple University; 2012. Available from: http://digital.library.temple.edu/u?/p245801coll10,214814

Université Montpellier II

4. Francois, Amaury. Distributions et fonctions du canal Calcique Cav3.2 dans les voies somatosensorielles : Cav3.2 Calcium Channel distribution and functions in somatosensory pathways.

Degree: Docteur es, Biologie Santé, 2013, Université Montpellier II

URL: http://www.theses.fr/2013MON20036

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Le traitement et la gestion de la douleur sont depuis toujours une priorité pour le corps médical. Malgré leur importance pour la qualité de vie,… (more)

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Le traitement et la gestion de la douleur sont depuis toujours une priorité pour le corps médical. Malgré leur importance pour la qualité de vie, les analgésiques couramment utilisés possèdent un ratio bénéfice/risque faible. La recherche de nouveaux concepts thérapeutiques pour lutter contre la douleur est donc une priorité. Afin de répondre à ce besoin, il faut d'abord comprendre les mécanismes de la perception de la douleur ainsi que, plus globalement, ceux permettant de percevoir son environnement. Dans ce contexte, de nombreuses études ont mis en évidence l'implication du canal calcique à bas seuil Cav3.2 dans les voies de la transmission de l'information douloureuse. Il représente donc une cible de choix pour le traitement de la douleur mais l'identité des neurones exprimant ces canaux ainsi que la fonction de Cav3.2 dans la physiologie des neurones sensoriels étaient jusqu'à présent inconnues. Au cours de cette thèse nous avons dans un premier temps décrit un nouvel inhibiteur des canaux calciques à bas seuil : le TTA-A2. Nous avons ainsi démontré que le TTA-A2 est un inhibiteur spécifique des canaux Cav3.1, Cav3.2, et Cav3.3. Il permet de diminuer l'excitabilité des neurones sensoriels exprimant Cav3.2, ce qui provoque une analgésie sur des animaux sains et pathologiques. Dans un deuxième temps nous nous sommes servis de ce nouvel outil en parallèle d'un nouveau modèle murin possédant une étiquette fluorescente (Knock in GFP) sur le canal Cav3.2 pour explorer la localisation et la fonction de Cav3.2 dans les neurones sensoriels. Nous avons ainsi découvert que Cav3.2 est exprimé dans des mécanorécepteurs à bas seuil impliqués dans la perception des stimuli mécaniques et thermiques nocifs ou non-nocifs. Le canal en lui-même se trouve aux endroits clés de la genèse et de la propagation du message nerveux périphérique, et module le seuil et la vitesse de conduction des potentiels d'action. Replacé dans le contexte de la bibliographie, l'ensemble de nos résultats montre que Cav3.2 permet de donner la modalité à bas seuil aux neurones l'exprimant.

Pain management and treatment have always been a priority for life quality. Despite this fact, analgesics commonly used present a bad benefice/risk ratio. Discovery of new therapeutic concepts to fight pain is highly required. To complete this task, we first need to better understand pain perception mechanisms, and more globally, mechanisms involved in the perception of our environment. In this context, numerous studies have shown that low threshold calcium channels Cav3.2 are involved in pain information transmission. Thus, it represents a good target for the treatment of pain. However, neuronal identity of Cav3.2-expressing sensory neurons and Cav3.2 functions in neuronal physiology are unknown. During this PhD we first described a new low voltage activated channel antagonist named TTA-A2. We demonstrated that TTA-A2 is a powerful nanomolar specific agonist of Cav3.1, Cav3.2 and Cav3.3. This molecule is able to reduce excitability in sensory neurons expressing…

Advisors/Committee Members: Bourinet, Emmanuel (thesis director).

Subjects/Keywords: Canaux calciques de type-T; Douleur; Cav3.2; Mecanorecepteur à bas seuil; Gfp; Tta-a2; T-type calcium channel; Pain; Cav3.2; Low threshold mechanoreceptor; Gfp; Tta-a2

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

APA (6^th Edition):

Francois, A. (2013). Distributions et fonctions du canal Calcique Cav3.2 dans les voies somatosensorielles : Cav3.2 Calcium Channel distribution and functions in somatosensory pathways. (Doctoral Dissertation). Université Montpellier II. Retrieved from http://www.theses.fr/2013MON20036

Chicago Manual of Style (16^th Edition):

Francois, Amaury. “Distributions et fonctions du canal Calcique Cav3.2 dans les voies somatosensorielles : Cav3.2 Calcium Channel distribution and functions in somatosensory pathways.” 2013. Doctoral Dissertation, Université Montpellier II. Accessed April 18, 2021. http://www.theses.fr/2013MON20036.

MLA Handbook (7^th Edition):

Francois, Amaury. “Distributions et fonctions du canal Calcique Cav3.2 dans les voies somatosensorielles : Cav3.2 Calcium Channel distribution and functions in somatosensory pathways.” 2013. Web. 18 Apr 2021.

Vancouver:

Francois A. Distributions et fonctions du canal Calcique Cav3.2 dans les voies somatosensorielles : Cav3.2 Calcium Channel distribution and functions in somatosensory pathways. [Internet] [Doctoral dissertation]. Université Montpellier II; 2013. [cited 2021 Apr 18]. Available from: http://www.theses.fr/2013MON20036.

Council of Science Editors:

Francois A. Distributions et fonctions du canal Calcique Cav3.2 dans les voies somatosensorielles : Cav3.2 Calcium Channel distribution and functions in somatosensory pathways. [Doctoral Dissertation]. Université Montpellier II; 2013. Available from: http://www.theses.fr/2013MON20036

5. Voisin, Tiphaine. Développement d’une souris modèle pour l’étude de la modulation metal/redox du canal calcique Cav3.2 dans l’excitabilité neuronale et dans les voies de la douleur : Development of a mouse model to study the metal/redox modulation of Cav3.2 calcium channels in neuronal excitability and in the pain pathways.

Degree: Docteur es, Neurosciences, 2015, Montpellier

URL: http://www.theses.fr/2015MONTT037

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Les canaux de type T Cav3.2 sont des canaux calciques activés pour de faibles dépolarisations membranaires. Ils ont un rôle important dans la régulation de… (more)

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Les canaux de type T Cav3.2 sont des canaux calciques activés pour de faibles dépolarisations membranaires. Ils ont un rôle important dans la régulation de l’excitabilité neuronale, particulièrement dans les neurones des ganglions rachidiens dorsaux (DRG) où ils sont impliqués dans la transmission de la douleur. Il est établi que les canaux Cav3.2, natifs et recombinants, sont inhibés par de faibles concentrations de métaux divalents tels que le zinc et le nickel et qu’ils sont modulés par des agents oxydo-réducteurs. In vitro, la mutation ponctuelle de l’histidine 191 en glutamine (H191Q) diminue fortement la sensibilité du canal Cav3.2 pour ces différents composés et il est proposé que cette régulation joue un rôle physiologique. L’objectif de ce travail de thèse a été d’étudier l’impact physiologique de cette modulation sur l’excitabilité neuronale et dans la perception de la douleur. Pour ce faire, nous avons généré une souris knock-in (KI) portant la mutation H191Q sur Cav3.2. L’étude électrophysiologique a été réalisée sur une population de neurones de DRG particulière : les cellules D-hair qui sont des mécanorécepteurs exprimant de grands courants Cav3.2. Nous avons validé que la sensibilité des canaux Cav3.2 neuronaux des souris KI est diminuée pour le zinc, le nickel et l’ascorbate. Nous montrons que cette régulation modifiée favorise une augmentation de l’excitabilité de ces neurones. Pour étudier l’impact de cette modulation in vivo, nous avons effectué des études comportementales. Les souris KI ne présentent pas de différence dans la perception de la douleur mécanique et thermique, ni dans l’hyperalgésie induite par l’inflammation et la neuropathie. Toutefois, dans le test à la formaline les souris KI montrent une réponse exacerbée dans la phase tardive. En résumé, nous décrivons ici un modèle animal original pour l’étude de la régulation metal/redox du canal Cav3.2 et identifions un rôle de cette modulation dans l’excitabilité des neurones D-Hair. Nos résultats obtenus in vivo indiquent cependant que cette modulation des canaux Cav3.2 aurait un impact limité dans les voies de la douleur.

Cav3.2 T-type channels are low-voltage activated calcium channels. They have an important role in the regulation of neuronal excitability, particularly in neurons of the dorsal root ganglia (DRG) where they are involved in pain transmission. It is established that Cav3.2 channels are inhibited by low concentrations of divalent metals such as zinc and nickel, and are modulated by redox agents. In vitro, the histidine191-to-glutamine mutation (H191Q) greatly reduces the Cav3.2 channel sensitivity to these compounds and it is proposed that this regulation plays a physiological role. The objective of this thesis was to study the physiological impact of this modulation on neuronal excitability and pain perception. To do this, we generated a knock-in (KI) mouse carrying the H191Q mutation on Cav3.2. Electrophysiological study was carried out on a particular population of DRG neurons, the D-hair cells, which are…

Advisors/Committee Members: Lory, Philippe (thesis director).

Subjects/Keywords: Canaux calciques de type T; Douleur; Souris génétiquement modifiée; Cav3.2; Neurones de DRG; T-Type calcium channel; Pain; Genetically modified mouse; Cav3.2; DRG neurons

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

APA (6^th Edition):

Voisin, T. (2015). Développement d’une souris modèle pour l’étude de la modulation metal/redox du canal calcique Cav3.2 dans l’excitabilité neuronale et dans les voies de la douleur : Development of a mouse model to study the metal/redox modulation of Cav3.2 calcium channels in neuronal excitability and in the pain pathways. (Doctoral Dissertation). Montpellier. Retrieved from http://www.theses.fr/2015MONTT037

Chicago Manual of Style (16^th Edition):

Voisin, Tiphaine. “Développement d’une souris modèle pour l’étude de la modulation metal/redox du canal calcique Cav3.2 dans l’excitabilité neuronale et dans les voies de la douleur : Development of a mouse model to study the metal/redox modulation of Cav3.2 calcium channels in neuronal excitability and in the pain pathways.” 2015. Doctoral Dissertation, Montpellier. Accessed April 18, 2021. http://www.theses.fr/2015MONTT037.

MLA Handbook (7^th Edition):

Voisin, Tiphaine. “Développement d’une souris modèle pour l’étude de la modulation metal/redox du canal calcique Cav3.2 dans l’excitabilité neuronale et dans les voies de la douleur : Development of a mouse model to study the metal/redox modulation of Cav3.2 calcium channels in neuronal excitability and in the pain pathways.” 2015. Web. 18 Apr 2021.

Vancouver:

Voisin T. Développement d’une souris modèle pour l’étude de la modulation metal/redox du canal calcique Cav3.2 dans l’excitabilité neuronale et dans les voies de la douleur : Development of a mouse model to study the metal/redox modulation of Cav3.2 calcium channels in neuronal excitability and in the pain pathways. [Internet] [Doctoral dissertation]. Montpellier; 2015. [cited 2021 Apr 18]. Available from: http://www.theses.fr/2015MONTT037.

Council of Science Editors:

Voisin T. Développement d’une souris modèle pour l’étude de la modulation metal/redox du canal calcique Cav3.2 dans l’excitabilité neuronale et dans les voies de la douleur : Development of a mouse model to study the metal/redox modulation of Cav3.2 calcium channels in neuronal excitability and in the pain pathways. [Doctoral Dissertation]. Montpellier; 2015. Available from: http://www.theses.fr/2015MONTT037

6. Barceló Gómez, Carla. Modulació de l'autofàgia com a nova estratègia terapèutica en el melanoma. Estudi de les resistències a fàrmacs convencionals.

Degree: Departament de Medicina, 2019, Universitat de Lleida

URL: http://hdl.handle.net/10803/666908

► Melanoma is a malignant neoplasia derived from melanocytes that once disseminated becomes highly resistant to chemotherapy and is associated with poor prognosis. Around 50% of… (more)

▼ Melanoma is a malignant neoplasia derived from melanocytes that once disseminated becomes highly resistant to chemotherapy and is associated with poor prognosis. Around 50% of melanomas carry the BRAFV600E mutation. Targeting BRAF mutant kinase by inhibitors, such as Vemurafenib, reduce tumor burden in disseminated melanoma. However, acquired resistance very frequently develops and tumors begin to progress under treatment. In previous studies, we have reported that T-type calcium channels (TTCCs) are overexpressed in melanoma cells and play an important role in melanoma progression. Importantly, TTCC pharmacological blockers (Mibefradil and Pimozide) reduce proliferation and deregulate autophagy leading to apoptosis. Therefore, in the previous results section, we analyzed the role of autophagy during migration and invasion processes of melanoma cells. TTCCs Cav3.1 and LC3II protein are highly expressed in BRAFV600E both in cell lines and biopsies compared to NRASQ61 mutant melanomas. Pharmacological blockade or gene silencing of TTCCs and Chloroquine, inhibit the autophagic flux and impair the migration and invasion capabilities, specifically in BRAFV600E melanoma cells. Because of Snail1 plays an important role in motility and invasion of melanoma cells, we showed that Snail1 is strongly expressed in BRAFV600E melanoma cells and patient biopsies, and its expression decreases when autophagy is blocked. In the first part of this work, we investigated the impact of inhibiting TTCCs in Vemurafenib resistant BRAFV600E melanomas. The results indicate that TTCC Cav3.1 is highly expressed in all Vemurafenib resistant melanoma cell lines and human melanoma biopsies compared to their parental counterparts. Besides, in Vemurafenib resistent cells or biopsies, we observed higher LC3 protein levels, in turn, increased autophagy. Particularly, TTCC blocker, Mibefradil, induces apoptosis and impaires migration rates while inhibiting autophagy in Vemurafenib resistent cells cells in vitro and in mouse xenografts in vivo. In addition, combination therapy (Vem+Mib) reduced or restored cell viability and migration/invasion rates depending on PTEN status. Therefore, when PTEN is non-functional, there is a delay in the death induction and an inhibition of cell migration in combination therapy in Vemurafenib resistant cell lines. Finally, Mibefradil inhibits the acquisition of resistance in BRAFV600E melanoma cells in combination with Vemurafenib. Taken together, our results suggest TTCCs as targetable in Vemurafenib resistant BRAFV600E melanomas and open the possibility to explore TTCC inhibition as a tool to avoid the acquisition of resistance to this BRAF inhibitor. In the second part of the present word, we have evaluated the therapeutic potential of M-CSF neutralizing antibody during resistance acquisition to BRAFi of BRAFV600Emelanoma cells by conditioned media. First, supernatant of cell cultures from resistant melanomas induces therapy resistance and modulates the phenotype of parental cells. Furthermore, we have observed that… Advisors/Committee Members: c[email protected] (authoremail), false (authoremailshow), Martí Laborda, Rosa Ma. (director), Macià Armengol, Anna (director).

Subjects/Keywords: Melanoma; Canals de Calci Tipus T; Autofàgia; Resistències; Canales de Calcio Tipo T; Resistencias; T-type calcium channel; Autophagy; Resistance; Dermatologia; 616.5

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

APA (6^th Edition):

Barceló Gómez, C. (2019). Modulació de l'autofàgia com a nova estratègia terapèutica en el melanoma. Estudi de les resistències a fàrmacs convencionals. (Thesis). Universitat de Lleida. Retrieved from http://hdl.handle.net/10803/666908

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):

Barceló Gómez, Carla. “Modulació de l'autofàgia com a nova estratègia terapèutica en el melanoma. Estudi de les resistències a fàrmacs convencionals.” 2019. Thesis, Universitat de Lleida. Accessed April 18, 2021. http://hdl.handle.net/10803/666908.

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

MLA Handbook (7^th Edition):

Barceló Gómez, Carla. “Modulació de l'autofàgia com a nova estratègia terapèutica en el melanoma. Estudi de les resistències a fàrmacs convencionals.” 2019. Web. 18 Apr 2021.

Vancouver:

Barceló Gómez C. Modulació de l'autofàgia com a nova estratègia terapèutica en el melanoma. Estudi de les resistències a fàrmacs convencionals. [Internet] [Thesis]. Universitat de Lleida; 2019. [cited 2021 Apr 18]. Available from: http://hdl.handle.net/10803/666908.

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

Council of Science Editors:

Barceló Gómez C. Modulació de l'autofàgia com a nova estratègia terapèutica en el melanoma. Estudi de les resistències a fàrmacs convencionals. [Thesis]. Universitat de Lleida; 2019. Available from: http://hdl.handle.net/10803/666908

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

Freie Universität Berlin

7. Bartolini, Laura. Calcium Signalling during Primary Angiogenic Sprouting in Zebrafish.

Degree: 2020, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-28123

► Die Angiogenese, die Entstehung neuer Blutgefäße aus vorbestehenden Blutgefäßen, stellt einen wichtigen Schritt bei der Formation eines funktionalen vaskulären Systems während der embryonalen Entwicklung dar.… (more)

▼ Die Angiogenese, die Entstehung neuer Blutgefäße aus vorbestehenden Blutgefäßen, stellt einen wichtigen Schritt bei der Formation eines funktionalen vaskulären Systems während der embryonalen Entwicklung dar. Fehlregulierungen bei der Entstehung des vaskulären Geflechts sind außerdem mit einer Vielzahl von Krankheiten, wie Krebs, Herzinfarkt und Schlaganfällen und Augenerkrankungen wie Makuladegeneration und mehr als 70 anderen Krankheiten assoziiert. Sowohl in vitro als auch in vivo Studien an Endothelzellen (EZ) zeigten einen wichtigen Einfluss des Vascular endothelial growth factor - (VEGF) Signalweges sowie der Aktivierung des Dll4/Notch-Signalweges auf die Regulierung der Differenzierung von EZ zu Spitzen- oder Stielzellen, auf die Migration von EZ sowie deren Proliferation während der Angiogenese. Gemeinsamkeiten zwischen der endothelialen Spitzenzelle und dem axonalen Wachstumskegel sind seit langem bekannt. Die beiden Zelltypen weisen nicht nur eine ähnliche anatomische Struktur, sondern auch gemeinsame molekulare Signalwege auf und reagieren auf dieselben Botenstoffe. Die Signaltransduktion durch Calciumionen, vorallem über den L-Typ Calciumkanal (LTCC), spielt eine wichtige Rolle bei der axonalen Wegfindung und beeinflusst entweder die Anziehung oder die Abstoßung der axonalen Zelle als Antwort auf Botenstoffe. In EZ ist ein Anstieg der zytosolischen Calcium-Konzentration (Ca2+i) unter anderem ein Schlüsselreiz für die Migration, Proliferation und Kontraktion der EZ sowie die Expression bestimmter Gene. Trotz der Gemeinsamkeiten zwischen dem neuronalen und vaskulären System, ist vor allem über die Rolle der Ca2+-Signaltransduktion über den LTCC bei der Formation des vaskulären Systems und der Angiogenese wenig bekannt. Die hier vorliegende Studie zeigt, dass der LTCC die Migration von EZ während der ersten angiogenetischen Aussprossung intersegmentaler Blutgefäße (ISV) in Zebrafisch-Embryonen reguliert. Eine Stimulation des LTCC führte zu einem starken Anstieg der Migration von EZ aus der dorsalen Aorta (DA) und resultierte in einer erhöhten Verzweigung entstehender Blutgefäße. Die Herunterregulation des Kanals reduzierte die Migration und Proliferation von EZ und führte zu einer Beeinträchtigung der Ausbildung von ISV. Des Weiteren konnte nachgewiesen werden, dass der LTCC bei der Entstehung von ISV synergistisch mit dem kanonischen transient receptor potential-1 (TRPC1) Ca2+-Kanal wechselwirkt, was die entscheidende Rolle des Ca2+-Fluxes durch die Plasmamembran während der Angiogenese beweist. Insgesamt zeigt die hier vorliegende Arbeit, dass Ca2+ - Ströme durch die Plasmamembran von Endothelzellen einen wichtigen Bestandteil des angiogenetischen Prozesses darstellen. Desweiteren ist für die Migration von Endothelzellen, wie beim axonalen Wachstumskegel, eine engmaschige Regulation von Calcium - Signalwegen vonnöten. Advisors/Committee Members: female (gender), Panáková, Daniela (firstReferee), Knaus, Petra (furtherReferee).

Subjects/Keywords: Calcium signalling; L-type Calcium Channel (LTCC); Angiogenesis; ddc:570

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

APA (6^th Edition):

Bartolini, L. (2020). Calcium Signalling during Primary Angiogenic Sprouting in Zebrafish. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-28123

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):

Bartolini, Laura. “Calcium Signalling during Primary Angiogenic Sprouting in Zebrafish.” 2020. Thesis, Freie Universität Berlin. Accessed April 18, 2021. http://dx.doi.org/10.17169/refubium-28123.

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

MLA Handbook (7^th Edition):

Bartolini, Laura. “Calcium Signalling during Primary Angiogenic Sprouting in Zebrafish.” 2020. Web. 18 Apr 2021.

Vancouver:

Bartolini L. Calcium Signalling during Primary Angiogenic Sprouting in Zebrafish. [Internet] [Thesis]. Freie Universität Berlin; 2020. [cited 2021 Apr 18]. Available from: http://dx.doi.org/10.17169/refubium-28123.

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

Council of Science Editors:

Bartolini L. Calcium Signalling during Primary Angiogenic Sprouting in Zebrafish. [Thesis]. Freie Universität Berlin; 2020. Available from: http://dx.doi.org/10.17169/refubium-28123

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

Wayne State University

8. Lu, Qi. Characterization Of High-Voltage-Activated Calcium Channels In Retinal Bipolar Cells.

Degree: PhD, Anatomy and Cell Biology, 2013, Wayne State University

URL: https://digitalcommons.wayne.edu/oa_dissertations/783

► Retinal bipolar cells, conveying visual information from photoreceptors to ganglion cells, segregate visual information into multiple parallel pathways through their diversified cell types and… (more)

▼ Retinal bipolar cells, conveying visual information from photoreceptors to ganglion cells, segregate visual information into multiple parallel pathways through their diversified cell types and physiological properties. Voltage-gated Ca²⁺ channels could be particularly important underlying the diversified physiological properties of different BCs. In this dissertation, I investigated the high-voltage-activated (HVA) calcium current in retinal bipolar cells in mice. In the first part of my dissertation, I characterized multiple bipolar cell-expressing GFP and/or Cre transgenic mouse lines. In the second part of my dissertation, by performing whole-cell patch-clamp recordings, I examined the electrophysiological properties of HVA calcium currents among CBCs and between CBCs and CBCs. In particular, the second part of my study focused on the investigation of electrophysiological, pharmacological, and molecular properties of HVA calcium currents in RBCs. The results of my studies showed that the HVA Ca²⁺ currents with different electrophysiological properties were observed among CBCs, and between CBCs and RBCs. First, large HVA Ca²⁺ currents were observed in OFF CBCs but not in ON-CBCs. Second, HVA Ca²⁺ currents among different bipolar cells were found to show different activation potentials. Furthermore, the HVA Ca²⁺ currents in RBCs exhibited two components, a sustained and a transient component with the latter activated at more negative potentials. My pharmacological results indicated the sustained and transient HVA Ca²⁺ currents are originated from L- and P/Q type Ca²⁺ channels, respectively. Using L-type Ca²⁺ channel knockout or deficient mouse lines, my results showed that the L-type Ca²⁺ currents in RBCs are mediated mainly by alpha1C Ca²⁺ channels with a minor component from alpha1F Ca²⁺ channels. The studies will advance our understanding of the role of voltage-gated Ca²⁺ channels in basic visual information processing in the retina as well as Ca²⁺ signaling and Ca²⁺ channel deficit-related diseases in the visual system. Advisors/Committee Members: Zhuo-Hua Pan.

Subjects/Keywords: L-type calcium channel; P/Q-type calcium channel; retina bipolar cell; type 4 cone bipolar cell; voltage gated calcium channel; Cell Biology; Ophthalmology; Physiology

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

APA (6^th Edition):

Lu, Q. (2013). Characterization Of High-Voltage-Activated Calcium Channels In Retinal Bipolar Cells. (Doctoral Dissertation). Wayne State University. Retrieved from https://digitalcommons.wayne.edu/oa_dissertations/783

Chicago Manual of Style (16^th Edition):

Lu, Qi. “Characterization Of High-Voltage-Activated Calcium Channels In Retinal Bipolar Cells.” 2013. Doctoral Dissertation, Wayne State University. Accessed April 18, 2021. https://digitalcommons.wayne.edu/oa_dissertations/783.

MLA Handbook (7^th Edition):

Lu, Qi. “Characterization Of High-Voltage-Activated Calcium Channels In Retinal Bipolar Cells.” 2013. Web. 18 Apr 2021.

Vancouver:

Lu Q. Characterization Of High-Voltage-Activated Calcium Channels In Retinal Bipolar Cells. [Internet] [Doctoral dissertation]. Wayne State University; 2013. [cited 2021 Apr 18]. Available from: https://digitalcommons.wayne.edu/oa_dissertations/783.

Council of Science Editors:

Lu Q. Characterization Of High-Voltage-Activated Calcium Channels In Retinal Bipolar Cells. [Doctoral Dissertation]. Wayne State University; 2013. Available from: https://digitalcommons.wayne.edu/oa_dissertations/783

9. Senatore, Adriano. Alternative splicing of Lymnaea Cav3 and NALCN ion channel genes serves to alter biophysical properties, membrane expression, and ion selectivity.

Degree: 2012, University of Waterloo

URL: http://hdl.handle.net/10012/6926

► Evidence is presented that Lymnaea contains homologues for mammalian Cav3 and NALCN 4-domain ion channels, which retain key amino acid sequence motifs that differentiate these… (more)

▼ Evidence is presented that Lymnaea contains homologues for mammalian Cav3 and NALCN 4-domain ion channels, which retain key amino acid sequence motifs that differentiate these channels from other 4-domain types. Molecular cloning and heterologous expression of the first invertebrate Cav3 channel cDNA from Lymnaea confirms that it indeed is a true homologue to mammalian Cav3 channels, retaining some hallmark biophysical and pharmacological features1. Interestingly, the Lymnaea Cav3 channel gene also exhibits alternative splicing that is conserved with mammalian Cav3.1 and Cav3.2 channels, with homologous exons 8b in the I-II linker (Cav3.1) and 25c in the III-IV linker (Cav3.1 and Cav3.2), that can selectively be included or omitted from the full length channel. We show that the developmental and spatial expression patterns of these splice variants are remarkably conserved, and that these splice variants produce analogous changes in membrane localization and biophysical properties when channels are expressed in HEK-293T cells. The Lymnaea Cav3 channel gene also undergoes alternative splicing in the domain II P-loop, with mutually exclusive exons 12A and 12B that code for a large portion of the P-loop just upstream of the selectivity filter. Such splicing is a novel discovery that is not conserved with vertebrates or any other deuterostome animal, all of which only contain 12A homologues of exon 12. However, protostome animals including Lymnaea stagnalis, Drosophila melanogaster, and C. elegans all have mutually exclusive 12A and 12B exons in their Cav3 channel genes. Evidence is presented that exon 12A is likely the ancestral exon for the domain II P-loop, and that alternate exon 12B evolved later. Furthermore, although the two Lymnaea variants possess the same selectivity filter motifs characteristic for Cav3 channels (i.e. EEDD), they exhibit dramatic differences in calcium vs. sodium selectivity, without significant differences in biophysical properties. This is the first account of alternative splicing used to modulate ion selectivity in a Cav3 channel homologue, and given that calcium is such an important electrogenic signaling molecule, these alterations are expected to have profound physiological implications. Amazingly, Lymnaea NALCN was also found to undergo alternative splicing in the domain II P-loop, but in this case, the entire P-loop is replaced by mutually exclusive exons 15a and 15b such that the selectivity filter is converted from the proposed non-selective sodium-permeable configuration (15b/EKEE; EEKE in mammals, nematodes and insects), to a calcium channel-like pore (15a/EEEE). Thorough phylogenetic analysis reveals that NALCN is extremely unconventional, in that alternative splicing has frequently and independently evolved to alter the selectivity filter in domains II or III, in multiple animal clades. Furthermore, the ancestral NALCN channel most likely contained an EEEE pore. This work brings into question NALCN’s proposed role as a major leak sodium conductance that depolarizes…

Subjects/Keywords: NALCN; Cav3; T-type; calcium; ion channel; Invertebrate; evolution; sodium

…5 1.3 Cav3 (T-type) voltage-gated calcium channels… …42 FIGURE 2. Singleton, snail T-type Ca2+ channel gene is distantly related to vertebrate… …between amino acid sequences of distant T-type channel homologs… …plasmid containing invertebrate T-type channel cDNA reveal highly abundant channels and… …65 Figure 2. T-type calcium channels utilize alternative 5’ donor splice sites to generate…

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APA (6^th Edition):

Senatore, A. (2012). Alternative splicing of Lymnaea Cav3 and NALCN ion channel genes serves to alter biophysical properties, membrane expression, and ion selectivity. (Thesis). University of Waterloo. Retrieved from http://hdl.handle.net/10012/6926

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):

Senatore, Adriano. “Alternative splicing of Lymnaea Cav3 and NALCN ion channel genes serves to alter biophysical properties, membrane expression, and ion selectivity.” 2012. Thesis, University of Waterloo. Accessed April 18, 2021. http://hdl.handle.net/10012/6926.

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

MLA Handbook (7^th Edition):

Senatore, Adriano. “Alternative splicing of Lymnaea Cav3 and NALCN ion channel genes serves to alter biophysical properties, membrane expression, and ion selectivity.” 2012. Web. 18 Apr 2021.

Vancouver:

Senatore A. Alternative splicing of Lymnaea Cav3 and NALCN ion channel genes serves to alter biophysical properties, membrane expression, and ion selectivity. [Internet] [Thesis]. University of Waterloo; 2012. [cited 2021 Apr 18]. Available from: http://hdl.handle.net/10012/6926.

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

Council of Science Editors:

Senatore A. Alternative splicing of Lymnaea Cav3 and NALCN ion channel genes serves to alter biophysical properties, membrane expression, and ion selectivity. [Thesis]. University of Waterloo; 2012. Available from: http://hdl.handle.net/10012/6926

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

10. Guan, Wendy. Domain II (S5-P) region in Lymnaea T-type calcium channels and its role in determining biophysical properties, ion selectivity and drug sensitivity.

Degree: 2014, University of Waterloo

URL: http://hdl.handle.net/10012/8507

► Invertebrate T-type calcium channels cloned from the great pond snail, Lymnaea Stagnalis (LCav3) possess highly sodium permeant ion channel currents by means of alternative splicing… (more)

Subjects/Keywords: Ion channels; Electrophysiology; T-type calcium channel; Cav3; Invertebrate; Evolution

…Depiction of T-type calcium channel structure: A single long polypeptide containing four domains… …gating kinetics in T-type calcium channels and stabilizes the channel in a closed state, in a… …119 4.10 Possible structural similarities between K2P and KIR and T-type calcium channels… …4 Figure 1.3 Structural determinants of a T-type channel… …type channel LCav3 and the calcium-selective L-type channel LCav1…

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APA (6^th Edition):

Guan, W. (2014). Domain II (S5-P) region in Lymnaea T-type calcium channels and its role in determining biophysical properties, ion selectivity and drug sensitivity. (Thesis). University of Waterloo. Retrieved from http://hdl.handle.net/10012/8507

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):

Guan, Wendy. “Domain II (S5-P) region in Lymnaea T-type calcium channels and its role in determining biophysical properties, ion selectivity and drug sensitivity.” 2014. Thesis, University of Waterloo. Accessed April 18, 2021. http://hdl.handle.net/10012/8507.

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

MLA Handbook (7^th Edition):

Guan, Wendy. “Domain II (S5-P) region in Lymnaea T-type calcium channels and its role in determining biophysical properties, ion selectivity and drug sensitivity.” 2014. Web. 18 Apr 2021.

Vancouver:

Guan W. Domain II (S5-P) region in Lymnaea T-type calcium channels and its role in determining biophysical properties, ion selectivity and drug sensitivity. [Internet] [Thesis]. University of Waterloo; 2014. [cited 2021 Apr 18]. Available from: http://hdl.handle.net/10012/8507.

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

Council of Science Editors:

Guan W. Domain II (S5-P) region in Lymnaea T-type calcium channels and its role in determining biophysical properties, ion selectivity and drug sensitivity. [Thesis]. University of Waterloo; 2014. Available from: http://hdl.handle.net/10012/8507

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

University of British Columbia

11. Hildebrand, Michael Earl. Differential modulation of T-type voltage gated calcium channels by G-protein coupled receptors.

Degree: PhD, Neuroscience, 2008, University of British Columbia

URL: http://hdl.handle.net/2429/1019

► T-type voltage-gated calcium (Ca2+) channels play critical roles in controlling neuronal excitability, firing patterns, and synaptic plasticity, although the mechanisms and extent to which T-type… (more)

▼ T-type voltage-gated calcium (Ca2+) channels play critical roles in controlling neuronal excitability, firing patterns, and synaptic plasticity, although the mechanisms and extent to which T-type Ca2+ channels are modulated by G-protein coupled receptors (GPCRs) remains largely unexplored. Investigations into T-type modulation within native neuronal systems have been complicated by the presence of multiple GPCR subtypes and a lack of pharmacological tools to separate currents generated by the three T-type isoforms; Cav3.1, Cav3.2, and Cav3.3. We hypothesize that specific Cav3 subtypes play unique roles in neuronal physiology due to their differential functional coupling to specific GPCRs. Co-expression of T-type channel subtypes and GPCRs in a heterologous system allowed us to identify the specific interactions between muscarinic acetylcholine (mAChR) or metabotropic glutamate (mGluR) GPCRs and individual Cav3 isoforms. Perforated patch recordings demonstrated that activation of Galpha<q/11>-coupled GPCRs had a strong inhibitory effect on Cav3.3 T-type Ca2+ currents but either no effect or a stimulating effect on Cav3.1 and Cav3.2 peak current amplitudes. Further study of the inhibition of Cav3.3 channels by a specific Galpha<q/11>-coupled mAChR (M1) revealed that this reversible inhibition was associated with a concomitant increase in inactivation kinetics. Pharmacological and genetic experiments indicated that the M1 receptor-mediated inhibition of Cav3.3 occurs specifically through a Galpha<q/11> signaling pathway that interacts with two distinct regions of the Cav3.3 channel. As hypothesized, the potentiation of Cav3.1 channels by a Galpha<q/11>-coupled mGluR (mGluR1) initially characterized in the heterologous system was also observed in a native neuronal system: the cerebellar Purkinje cell (PC). In recordings on PCs within acute cerebellar slices, we demonstrated that the potentiation of Cav3.1 currents by mGluR1 activation is strongest near the threshold of T-type currents, enhancing the excitability of PCs. Ultrafast two-photon Ca2+ imaging demonstrated that the functional coupling between mGluR1 and T-type transients occurs within dendritic spines, where synaptic integration and plasticity occurs. A subset of these experiments utilized physiological synaptic activation and specific mGluR1 antagonists in wild-type and Cav3.1 knock-out mice to show that the mGluR1-mediated potentiation of Cav3.1 T-type currents may promote synapse-specific Ca2+ signaling in response to bursts of excitatory inputs.

Subjects/Keywords: T-type modulation; Calcium channel receptor; Glutamate; Acetylcholine; Purkinje cell; Electrophysiology

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

APA (6^th Edition):

Hildebrand, M. E. (2008). Differential modulation of T-type voltage gated calcium channels by G-protein coupled receptors. (Doctoral Dissertation). University of British Columbia. Retrieved from http://hdl.handle.net/2429/1019

Chicago Manual of Style (16^th Edition):

Hildebrand, Michael Earl. “Differential modulation of T-type voltage gated calcium channels by G-protein coupled receptors.” 2008. Doctoral Dissertation, University of British Columbia. Accessed April 18, 2021. http://hdl.handle.net/2429/1019.

MLA Handbook (7^th Edition):

Hildebrand, Michael Earl. “Differential modulation of T-type voltage gated calcium channels by G-protein coupled receptors.” 2008. Web. 18 Apr 2021.

Vancouver:

Hildebrand ME. Differential modulation of T-type voltage gated calcium channels by G-protein coupled receptors. [Internet] [Doctoral dissertation]. University of British Columbia; 2008. [cited 2021 Apr 18]. Available from: http://hdl.handle.net/2429/1019.

Council of Science Editors:

Hildebrand ME. Differential modulation of T-type voltage gated calcium channels by G-protein coupled receptors. [Doctoral Dissertation]. University of British Columbia; 2008. Available from: http://hdl.handle.net/2429/1019

12. Temme, Stephanie A. J. Maladaptive Fear and L-type Voltage Gated Calcium Channel Subtypes.

Degree: PhD, Neuroscience, 2015, University of Michigan

URL: http://hdl.handle.net/2027.42/111524

► Fear learning can be adaptive and maladaptive. Learned fear to a harmful stimulus is adaptive and helps organisms survive in a given environment. However, learned… (more)

▼ Fear learning can be adaptive and maladaptive. Learned fear to a harmful stimulus is adaptive and helps organisms survive in a given environment. However, learned fear can be maladaptive when it is persistent or when it is generalized to a non-threatening stimulus. These types of fears are often diagnosed as trauma or anxiety-related disorders in humans. Despite being the number one most common mental health disorder in the United States, very little is understood about the formation of these disorders and underlying maladaptive fears. Studies have implicated a class of voltage-gated calcium channels (VGCCs), known as L-type VGCCs (LVGCCs), in both the formation and extinction of conditioned fear. Additionally, LVGCCs have been linked to changes in the neuronal plasticity in structures known to be involved in fear learning including the amygdala and the hippocampus. While it is clear that LVGCCs are involved with these forms of fear related learning, it is not clear to what extent LVGCCs and the two LVGCC neuronal subtypes, CaV1.2 and CaV1.3, mediate adaptive and maladaptive fears or the neurophysiology associated with fear. Understanding the contribution of these LVGCCs to maladaptive fear learning could provide insights into the neurobiological mechanism underlying trauma and anxiety-related disorders. The goal of the research presented in this thesis was to investigate adaptive and maladaptive fear phenotypes, as well as explore the individual role of CaV1.2 and CaV1.3 in fear related learning and physiology. Utilizing mice with a conditional knockout of CaV1.2 in neurons in the brain, mice with a global knockout of CaV1.3, and various pure-bred mouse strains and sub-strains, five main points are illustrated: 1) Two forms of maladaptive fear learning, persistent fear and generalized fear exist, 2) CaV1.2 mediates generalized fear, likely through the dentate gyrus and adult neurogenesis, 3) CaV1.2 mediates persistent fear, likely through alterations in the inhibitory/excitatory synaptic activity onto the amygdala. 4) Deletion of CaV1.2 alters neurophysiological correlates of learning in the amygdala, including intrinsic excitability and synaptic plasticity. 5) CaV1.2 appears to alter behavior and neurophysiology in a LVGCC subtype specific manner. Advisors/Committee Members: Murphy, Geoffrey G. (committee member), Stuenkel, Edward L. (committee member), Isom, Lori (committee member), Sutton, Michael Mark Alexander (committee member), Seasholtz, Audrey (committee member).

Subjects/Keywords: fear; calcium channel; L-type; Neurosciences; Health Sciences

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APA (6^th Edition):

Temme, S. A. J. (2015). Maladaptive Fear and L-type Voltage Gated Calcium Channel Subtypes. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/111524

Chicago Manual of Style (16^th Edition):

Temme, Stephanie A J. “Maladaptive Fear and L-type Voltage Gated Calcium Channel Subtypes.” 2015. Doctoral Dissertation, University of Michigan. Accessed April 18, 2021. http://hdl.handle.net/2027.42/111524.

MLA Handbook (7^th Edition):

Temme, Stephanie A J. “Maladaptive Fear and L-type Voltage Gated Calcium Channel Subtypes.” 2015. Web. 18 Apr 2021.

Vancouver:

Temme SAJ. Maladaptive Fear and L-type Voltage Gated Calcium Channel Subtypes. [Internet] [Doctoral dissertation]. University of Michigan; 2015. [cited 2021 Apr 18]. Available from: http://hdl.handle.net/2027.42/111524.

Council of Science Editors:

Temme SAJ. Maladaptive Fear and L-type Voltage Gated Calcium Channel Subtypes. [Doctoral Dissertation]. University of Michigan; 2015. Available from: http://hdl.handle.net/2027.42/111524

Texas A&M University

13. Huang, Chia-Yu. Circadian Regulation of L-Type Voltage-Gated Calcium Channels in Avian Retina.

Degree: PhD, Biomedical Sciences, 2014, Texas A&M University

URL: http://hdl.handle.net/1969.1/153808

► The circadian clock is an endogenous time-keeping mechanism that allows an organism to synchronize itself with external time cues and prepares the organism to anticipate… (more)

▼ The circadian clock is an endogenous time-keeping mechanism that allows an organism to synchronize itself with external time cues and prepares the organism to anticipate upcoming environmental changes on a daily basis. The retina is a light-sensitive neuronal tissue located in the back of the eye. The circadian clocks in the retina enable the retina to anticipate daily ambient illumination over at least twelve orders of magnitude and initiate the adaptive processes with visual system throughout the course of a day. The retinal photoreceptors are responsible for phototransduction and transmitting the visual information into the brain. Unlike most neurons, photoreceptors do not fire action potentials, and they release neurotransmitter in a sustained manner, which is governed by the L-type voltage-gated calcium channels (L-VGCCs). The mRNA and protein expression of the α1 pore forming subunit of L-VGCCs are under circadian control, in which the protein expression of L-VGCCα1 with a corresponding increase in the L-VGCC current density is higher at night than during the day. Using the chicken embryo as a model system, an integrative strategy was used through combining biochemical, molecular, morphological, and electrophysiological analyses to investigate cellular mechanisms of the circadian regulation of L-VGCCs in the photoreceptors. Three important cell signaling molecules and their pathways were investigated in this dissertation: calcineurin, mechanistic/mammalian target of rapamycin complex 1 (mTORC1), and AMP-activated protein kinase (AMPK). The activities of the protein phosphatase calcineurin, as well as the protein kinase mTORC1 exhibited circadian oscillation with their activities higher at night than during the day, while the activities of AMPK are greater during the day compared to the activities at night. Inhibition of calcineurin and mTORC1 dampened the current densities and protein expression of L-VGCCs at night, while activation of AMPK decreased L-VGCC currents at night. These signaling molecules interacted with cAMP-Ras-MAPK and cAMP-Ras-PI3K-AKT signaling pathways to modulate the L-VGCC trafficking from the cytosol onto the plasma membrane in a circadian phase-dependent manner. The results demonstrated that the complex of cellular signaling pathways participated in the circadian regulation of L-VGCCs in the photoreceptors. Understanding the molecular mechanism underlying the circadian regulation of L-VGCCs in cone photoreceptors will provide important knowledge on how circadian clocks regulate retinal physiology and function in healthy states. Changes in L-VGCCs and these cell-signaling molecules might be indicators or biomarkers for age-related macular degeneration or other retinal degenerative diseases. Advisors/Committee Members: Ko, Gladys (advisor), Abbott , Louise (committee member), Tiffany-Castiglioni, Evelyn (committee member), Griffith, William (committee member).

Subjects/Keywords: Circadian; Retina; L-type voltage-gated calcium channel; Signal transduction

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

APA (6^th Edition):

Huang, C. (2014). Circadian Regulation of L-Type Voltage-Gated Calcium Channels in Avian Retina. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/153808

Chicago Manual of Style (16^th Edition):

Huang, Chia-Yu. “Circadian Regulation of L-Type Voltage-Gated Calcium Channels in Avian Retina.” 2014. Doctoral Dissertation, Texas A&M University. Accessed April 18, 2021. http://hdl.handle.net/1969.1/153808.

MLA Handbook (7^th Edition):

Huang, Chia-Yu. “Circadian Regulation of L-Type Voltage-Gated Calcium Channels in Avian Retina.” 2014. Web. 18 Apr 2021.

Vancouver:

Huang C. Circadian Regulation of L-Type Voltage-Gated Calcium Channels in Avian Retina. [Internet] [Doctoral dissertation]. Texas A&M University; 2014. [cited 2021 Apr 18]. Available from: http://hdl.handle.net/1969.1/153808.

Council of Science Editors:

Huang C. Circadian Regulation of L-Type Voltage-Gated Calcium Channels in Avian Retina. [Doctoral Dissertation]. Texas A&M University; 2014. Available from: http://hdl.handle.net/1969.1/153808

Texas A&M University

14. Nigussie, Fikru. Analysis of Hippocampal Cell Proliferation, Survival, and Neuronal Morphology in P/Q-Type Voltage-Gated Calcium Channel Mutant Mice.

Degree: PhD, Biomedical Sciences, 2013, Texas A&M University

URL: http://hdl.handle.net/1969.1/149268

► Tottering and leaner mutant mice carry mutations in the pore-forming subunit (1A) of P/Q-type (CaV 2.1) voltage-gated calcium ion (Ca2+) channels that result in reduced… (more)

▼ Tottering and leaner mutant mice carry mutations in the pore-forming subunit (1A) of P/Q-type (CaV 2.1) voltage-gated calcium ion (Ca2+) channels that result in reduced Ca2+ current density. Since Ca2+ influx via voltage-dependent Ca2+ channels regulates important Ca2+-dependent neuronal processes including neurotransmitter release and synaptogenesis, we assessed effects of these mutations on hippocampus volume, neuronal density, neuronal morphology of hippocampal pyramidal cells in adult (six-month-old) mice, and adult neurogenesis in three-week-old and six-month-old mice. Hippocampal volume and neuronal density were assessed using hematoxylin and eosin stained serial sections. Neuronal morphology was assessed using Golgi-Cox staining as well as ultrastructural assessment using transmission electron microscopy. Adult hippocampal neurogenesis was assessed using standard 5-bromo-2’-deoxyuridine (BrdU) labeling with fluorescent immunohistochemistry (IHC) and proliferating cell nuclear antigen (PCNA) with diaminobenzidine IHC. To determine neuron and astrocyte survival, we used fluorescent double labeling for neurons with BrdU-neuronal nuclei IHC or astrocytes using BrdU-glial fibrillary acidic protein, respectively. Fluoro-Jade histochemistry was used to assess numbers of degenerating cells in the dentate gyrus subgranular zone. Decreased hippocampus volume was observed in tottering female mice and increased dentate hilar and CA1 cell density in mutant mice compared to wild type mice. Cell proliferation was increased in the hilus and combined CA3, CA2 and CA1 regions of mutant mice compared to wild type mice. Decreased total dendritic length and decreased number of dendritic intersections was observed in tottering mice compared to wild type mice. The decrease in dendritic arborization of tottering mice occurred at the concentric circles close to the neuronal cell body indicating that basal dendrites of CA1 pyramidal neurons are reduced. Taken together, P/Q-type voltage gated calcium channel mutation has age variable influence on adult hippocampal cell proliferation, and it altered neuronal morphology in terms of dendritic complexity in tottering mice, while the leaner mutation reduced mitochondrial density. Advisors/Committee Members: Abbott, Louise C (advisor), Winzer-Serhan, Ursula H (committee member), Welsh, C Jane (committee member), Stoica, George (committee member).

Subjects/Keywords: Tottering; Leaner; P/Q-type calcium channel; hippocampus

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APA (6^th Edition):

Nigussie, F. (2013). Analysis of Hippocampal Cell Proliferation, Survival, and Neuronal Morphology in P/Q-Type Voltage-Gated Calcium Channel Mutant Mice. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/149268

Chicago Manual of Style (16^th Edition):

Nigussie, Fikru. “Analysis of Hippocampal Cell Proliferation, Survival, and Neuronal Morphology in P/Q-Type Voltage-Gated Calcium Channel Mutant Mice.” 2013. Doctoral Dissertation, Texas A&M University. Accessed April 18, 2021. http://hdl.handle.net/1969.1/149268.

MLA Handbook (7^th Edition):

Nigussie, Fikru. “Analysis of Hippocampal Cell Proliferation, Survival, and Neuronal Morphology in P/Q-Type Voltage-Gated Calcium Channel Mutant Mice.” 2013. Web. 18 Apr 2021.

Vancouver:

Nigussie F. Analysis of Hippocampal Cell Proliferation, Survival, and Neuronal Morphology in P/Q-Type Voltage-Gated Calcium Channel Mutant Mice. [Internet] [Doctoral dissertation]. Texas A&M University; 2013. [cited 2021 Apr 18]. Available from: http://hdl.handle.net/1969.1/149268.

Council of Science Editors:

Nigussie F. Analysis of Hippocampal Cell Proliferation, Survival, and Neuronal Morphology in P/Q-Type Voltage-Gated Calcium Channel Mutant Mice. [Doctoral Dissertation]. Texas A&M University; 2013. Available from: http://hdl.handle.net/1969.1/149268

15. F. Rusconi. THE IMPORTANT ROLE OF AKT IN THE MODULATION OF HEART INOTROPISM THROUGH L-TYPE CALCIUM CHANNELS FUNCTION.

Degree: 2010, Università degli Studi di Milano

URL: http://hdl.handle.net/2434/150100

► The insulin IGF1/Akt signaling pathway has recently been shown to be critical for the regulation of heart function and physiology. Indeed, compelling evidence shows activation… (more)

▼ The insulin IGF1/Akt signaling pathway has recently been shown to be critical for the regulation of heart function and physiology. Indeed, compelling evidence shows activation of this pathway as one of the most important determinants for the enhancement of cardiac function and physiological growth in athletes, whereas its impairment is considered critical for the development of heart failure (HF). In this doctoral thesis, our aim was to determine the functional role of known and novel key-factors of this pathway to study whether their modulation might be envisaged as therapeutic tool for curing pathological cardiac hypertrophy (CH) and HF. Physiological CH is an adaptive response of the heart to stimuli, such as developmental growth and training and differs markedly from pathological hypertrophy occurring in patients with HF. In this thesis, we demonstrated the involvement of Akt kinase in regulating heart inotropism by modulating L-Type Ca2+ Channel (LTCC) density and function. In a mouse model with inducible and cardiac specific deletion of PDK1, the upstream activator of Akt, we found that the protein stability of the LTCC pore subunit (Cavα1) can be modulated by the kinase. In particular, phosphorylation of the C-terminal coiled coil of the Cavβ2 chaperone subunit enhances LTCC protein stability by prevention of PEST-mediated Cavα1 degradation. Subsequently, to determine whether the modulation of this mechanism may be used for the treatment of HF, we studied the fine-regulation of LTCC density and activity by investigating the functional role of Akt-phosphomimetics Cavβ2 constructs. Three Akt-phosphomimetic sequences corresponding to the Cavβ2 C-terminal coiled coil were identified and shown to protect Cavα1 from protein degradation, through an increase in the number of functional LTCC. Moreover, to establish whether the Akt-dependent phosphorylation of CaVβ2 might be a trigger for the recruitment of other protein interacting partners, yeast two-hybrid screenings of human and mouse heart cDNA expression libraries revealed a fold-back interaction of the Akt-phosphorylated-Cavβ2 tail with a region of the Cavβ2 globular domain. Co-immunoprecipitation experiments confirmed this interaction, while negative results were obtained when Cavβ2-WT was used as bait. This provided the proof of concept for a mechanism of action that relies on Akt-dependent phosphorylation. Site-specific mutagenesis in the identified interacting domain confirmed this mechanism. All togheter, we found that the Akt-dependent protective effect on Cavα1 stability might relay on Cavβ2 structural rearrangements, which follow the phosphorylated C-terminal coiled coil fold back on its globular domain. In conclusion, results from this doctoral thesis provide further insights into the role of the insulin IGF1/Akt signaling pathway and its role in the modulation of myocardial physiology and HF. These findings may lead to the development of new therapeutical tools that will be useful for the modulation of impaired cardiac contractility in HF. Advisors/Committee Members: tutor: Dario Di Francesco, coordinatore: Paolo Cavallari, supervisor: Gianluigi Condorelli, supervisor: Daniele Catalucci, DI FRANCESCO, DARIO, CAVALLARI, PAOLO.

Subjects/Keywords: Akt; L-type Calcium channel; heart failure; Settore BIO/09 - Fisiologia

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

APA (6^th Edition):

Rusconi, F. (2010). THE IMPORTANT ROLE OF AKT IN THE MODULATION OF HEART INOTROPISM THROUGH L-TYPE CALCIUM CHANNELS FUNCTION. (Thesis). Università degli Studi di Milano. Retrieved from http://hdl.handle.net/2434/150100

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):

Rusconi, F.. “THE IMPORTANT ROLE OF AKT IN THE MODULATION OF HEART INOTROPISM THROUGH L-TYPE CALCIUM CHANNELS FUNCTION.” 2010. Thesis, Università degli Studi di Milano. Accessed April 18, 2021. http://hdl.handle.net/2434/150100.

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

MLA Handbook (7^th Edition):

Rusconi, F.. “THE IMPORTANT ROLE OF AKT IN THE MODULATION OF HEART INOTROPISM THROUGH L-TYPE CALCIUM CHANNELS FUNCTION.” 2010. Web. 18 Apr 2021.

Vancouver:

Rusconi F. THE IMPORTANT ROLE OF AKT IN THE MODULATION OF HEART INOTROPISM THROUGH L-TYPE CALCIUM CHANNELS FUNCTION. [Internet] [Thesis]. Università degli Studi di Milano; 2010. [cited 2021 Apr 18]. Available from: http://hdl.handle.net/2434/150100.

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

Council of Science Editors:

Rusconi F. THE IMPORTANT ROLE OF AKT IN THE MODULATION OF HEART INOTROPISM THROUGH L-TYPE CALCIUM CHANNELS FUNCTION. [Thesis]. Università degli Studi di Milano; 2010. Available from: http://hdl.handle.net/2434/150100

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

Colorado State University

16. Dang, An Khanh. Regulation of local L-type calcium channel signaling in anterior pituitary gonadotropes.

Degree: PhD, Biomedical Sciences, 2017, Colorado State University

URL: http://hdl.handle.net/10217/185697

► The binding of gonadotropin-releasing hormone (GnRH) to its receptor initiates signaling cascades in gonadotropes which result in enhanced luteinizing hormone (LH) and follicle stimulating hormone… (more)

▼ The binding of gonadotropin-releasing hormone (GnRH) to its receptor initiates signaling cascades in gonadotropes which result in enhanced luteinizing hormone (LH) and follicle stimulating hormone (FSH) biosynthesis and secretion. Most dramatic is the sharp rise in LH secretion ("LH surge") that precedes and is necessary for follicular maturation and ovulation. Ca2+ influx activates mitogen-activated protein kinases (MAPKs) which lead to increased transcription of LH and FSH genes. Interestingly, previous research suggests that two MAPK signaling pathways, ERK and JNK, are activated by either Ca2+ influx through L-type Ca2+ channels or by global Ca2+ signals originating from intracellular stores, respectively. These discrete Ca2+ sources for divergent signaling cascades provides a mechanism in which gonadotropes can decode different pathways for appropriate gonadotropin release during various stages of the ovulatory cycle. However, direct evidence supporting an underlying subplasmalemmal local Ca2+ signaling through L-type Ca2+ channels distinct from intracellular Ca2+ was lacking. Here we used a combination of electrophysiology and total internal reflection fluorescence (TIRF) microscopy to visualize discrete sites of Ca2+ influx (Ca2+ sparklets) in gonadotrope-derived αT3-1 cells in real time. These localized GnRH-induced Ca2+ influxes are mediated by L-type Ca2+ channels and important for downstream ERK activation. In addition, precise structural and molecular elements to create a microenvironment suitable for localized subplasmalemmal L-type Ca2+ channel signaling was necessary for gonadotrope function, in which GnRH-dependent stimulation of L-type Ca2+ channel influx was found to require PKC and a dynamic actin cytoskeleton. More recently, we have further elucidated molecular mechanisms modulating localized L-type Ca2+ channel influx. Reactive oxygen species (ROS) are cognate signaling molecules that mediate cell function, but their role in regulating Ca2+ in gonadotropes is unknown. We have explored GnRH regulation of both NADPH oxidase complexes and mitochondrial sources of ROS and assessed ROS modulation of L-type Ca2+ channel activity in gonadotropes. We identified GnRH-induced spatially localized ROS "puncta" in αT3-1 cells, and ROS increased local Ca2+ channel activity in both αT3-1 cells and primary mouse gonadotropes. In addition, GnRH increased mitochondrial oxidation activity at the subplasmalemmal surface and mitochondrial ROS increased localized L-type Ca2+ channel influx. Also, active L-type Ca2+ channels were associated with subplasmalemmal mitochondria. Taken together, this dissertation explored the first direct evidence for localized L-type Ca2+ channel signaling in αT3-1 cells and elucidated signaling mechanisms in gonadotropes. Specifically, cellular organization via an intact cytoskeletal platform and ROS regulated L-type Ca2+ channel sparklet activity that are important for the downstream ERK activation and gonadotropin gene expression that regulates reproduction. Advisors/Committee Members: Amberg, Greg (advisor), Clay, Colin (advisor), Tamkun, Michael (committee member), Navratil, Amy (committee member), Duval, Dawn (committee member).

Subjects/Keywords: gonadotrope; reactive oxygen species; GnRH; reproductive endocrinology; L-type calcium channel

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

APA (6^th Edition):

Dang, A. K. (2017). Regulation of local L-type calcium channel signaling in anterior pituitary gonadotropes. (Doctoral Dissertation). Colorado State University. Retrieved from http://hdl.handle.net/10217/185697

Chicago Manual of Style (16^th Edition):

Dang, An Khanh. “Regulation of local L-type calcium channel signaling in anterior pituitary gonadotropes.” 2017. Doctoral Dissertation, Colorado State University. Accessed April 18, 2021. http://hdl.handle.net/10217/185697.

MLA Handbook (7^th Edition):

Dang, An Khanh. “Regulation of local L-type calcium channel signaling in anterior pituitary gonadotropes.” 2017. Web. 18 Apr 2021.

Vancouver:

Dang AK. Regulation of local L-type calcium channel signaling in anterior pituitary gonadotropes. [Internet] [Doctoral dissertation]. Colorado State University; 2017. [cited 2021 Apr 18]. Available from: http://hdl.handle.net/10217/185697.

Council of Science Editors:

Dang AK. Regulation of local L-type calcium channel signaling in anterior pituitary gonadotropes. [Doctoral Dissertation]. Colorado State University; 2017. Available from: http://hdl.handle.net/10217/185697

17. Brennecke, Ashton. EVALUATING THE ROLE OF A CaV2.2 SPLICE VARIANT IN BEHAVIORAL RESPONSES TO STRESS, NOVELTY, AND OTHER MONOAMINE-LINKED FUNCTIONS.

Degree: MS, 2019, University of New Hampshire

URL: https://scholars.unh.edu/thesis/1319

► CaV2.2 (N-type) channel is a presynaptic channel that enables calcium influx into axon terminals, thereby playing a vital role in coupling action potentials to… (more)

Subjects/Keywords: Exon 18a; Monoamines; N-type calcium channel; Stress

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APA (6^th Edition):

Brennecke, A. (2019). EVALUATING THE ROLE OF A CaV2.2 SPLICE VARIANT IN BEHAVIORAL RESPONSES TO STRESS, NOVELTY, AND OTHER MONOAMINE-LINKED FUNCTIONS. (Thesis). University of New Hampshire. Retrieved from https://scholars.unh.edu/thesis/1319

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):

Brennecke, Ashton. “EVALUATING THE ROLE OF A CaV2.2 SPLICE VARIANT IN BEHAVIORAL RESPONSES TO STRESS, NOVELTY, AND OTHER MONOAMINE-LINKED FUNCTIONS.” 2019. Thesis, University of New Hampshire. Accessed April 18, 2021. https://scholars.unh.edu/thesis/1319.

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

MLA Handbook (7^th Edition):

Brennecke, Ashton. “EVALUATING THE ROLE OF A CaV2.2 SPLICE VARIANT IN BEHAVIORAL RESPONSES TO STRESS, NOVELTY, AND OTHER MONOAMINE-LINKED FUNCTIONS.” 2019. Web. 18 Apr 2021.

Vancouver:

Brennecke A. EVALUATING THE ROLE OF A CaV2.2 SPLICE VARIANT IN BEHAVIORAL RESPONSES TO STRESS, NOVELTY, AND OTHER MONOAMINE-LINKED FUNCTIONS. [Internet] [Thesis]. University of New Hampshire; 2019. [cited 2021 Apr 18]. Available from: https://scholars.unh.edu/thesis/1319.

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

Council of Science Editors:

Brennecke A. EVALUATING THE ROLE OF A CaV2.2 SPLICE VARIANT IN BEHAVIORAL RESPONSES TO STRESS, NOVELTY, AND OTHER MONOAMINE-LINKED FUNCTIONS. [Thesis]. University of New Hampshire; 2019. Available from: https://scholars.unh.edu/thesis/1319

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

18. Fruquiere, Antoine. Canaux calciques de type T spinaux et sensibilité douloureuse : Spinal T-type calcium channels and pain sensitivity.

Degree: Docteur es, Biologie Santé, 2018, Montpellier

URL: http://www.theses.fr/2018MONTT061

► Alors que la douleur physiologique est essentielle à la survie de l'individu, les douleurs chroniques sont purement délétères pour l'organisme et la qualité de la… (more)

▼ Alors que la douleur physiologique est essentielle à la survie de l'individu, les douleurs chroniques sont purement délétères pour l'organisme et la qualité de la vie. Malheureusement, les traitements actuels se limitent à des médicaments peu efficaces ou présentant un mauvais rapport bénéfice / risque. Il est donc urgent de mieux comprendre les mécanismes d'établissement et de persistance des douleurs chroniques, comme les douleurs neuropathiques, afin de concevoir des stratégies thérapeutiques efficaces contre ces pathologies. De nombreuses études ont montré que les canaux calciques de type T sont impliqués dans les états douloureux chroniques. Par exemple, le sous-type Cav3.2, est exprimé tout au long du circuit neuronal nociceptif. Dans le système nerveux périphérique, les canaux Cav3.2 ont un rôle pronociceptif et sont désormais validées comme cibles pour la recherche de thérapies innovantes. En revanche, le rôle du canal Cav3.2 au niveau central, et en particulier dans la moelle épinière, un point névralgique de convergence, d'intégration et de transmission des informations nociceptives, reste à explorer.Grâce à un modèle murin Cav3.2GFP-Lox knock-in créé par l'équipe, nous avons pu identifier/localiser précisément les neurones Cav3.2 positifs dans tout le système nerveux et induire une délétion tissulaire spécifique de Cav3.2 par l’action de la Cre recombinase, pour ensuite en évaluer les effets sur la sensibilité à la douleur. Dans la moelle épinière, nous avons constaté que Cav3.2 est fortement exprimé dans les neurones des laminae superficielles, et sont principalement des neurones excitateurs. La suppression de Cav3.2 spinal par une approche virale a démontré comportementalement : i) l’abolition de l’allodynie au froid et mécanique, de l’hyperalgésie mécanique, ainsi que des douleurs spontanées, en condition neuropathiques chez les mâles et les femelles, ii) une altération de la perception au chaud en condition neuropathique avec un effet différentiel dépendant du sexe, et iii) une réduction de l’anxiété associée aux douleurs chroniques, iv) la suppression des effets analgésiques d’un traitement systémique d’un bloqueur pharmacologique de canaux calciques de type T. Mécanistiquement, les enregistrements extracellulaires in vivo des neurones de projection spinaux démontrent une diminution de l'intégration et de la transmission des messages nociceptifs pathologiques des fibres périphériques C et A-delta lorsque le canal Cav3.2 est délété dans les réseaux spinaux. Cette approche de délétion a été développée avant et après l'induction du modèle de douleur neuropathique pour en évaluer les effets préventifs et curatifs.Les résultats démontrent que la délétion du canal spinal Cav3.2 a des effets préventifs et curatifs sur les symptômes des douleurs neuropathiques. Dans une perspective clinique pour le développement d'analgésiques basés sur les inhibiteurs calciques de type T, nous suggérons de cibler Cav3.2 spinal en plus des canaux dans les neurones afférents primaires par des molécules pénétrant le système… Advisors/Committee Members: Bourinet, Emmanuel (thesis director).

Subjects/Keywords: Douleurs chroniques; Moelle épinière; T-Type channel; Approche virale; Chronic pain; Spinal cord; T-Type channel; Viral approach

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

APA (6^th Edition):

Fruquiere, A. (2018). Canaux calciques de type T spinaux et sensibilité douloureuse : Spinal T-type calcium channels and pain sensitivity. (Doctoral Dissertation). Montpellier. Retrieved from http://www.theses.fr/2018MONTT061

Chicago Manual of Style (16^th Edition):

Fruquiere, Antoine. “Canaux calciques de type T spinaux et sensibilité douloureuse : Spinal T-type calcium channels and pain sensitivity.” 2018. Doctoral Dissertation, Montpellier. Accessed April 18, 2021. http://www.theses.fr/2018MONTT061.

MLA Handbook (7^th Edition):

Fruquiere, Antoine. “Canaux calciques de type T spinaux et sensibilité douloureuse : Spinal T-type calcium channels and pain sensitivity.” 2018. Web. 18 Apr 2021.

Vancouver:

Fruquiere A. Canaux calciques de type T spinaux et sensibilité douloureuse : Spinal T-type calcium channels and pain sensitivity. [Internet] [Doctoral dissertation]. Montpellier; 2018. [cited 2021 Apr 18]. Available from: http://www.theses.fr/2018MONTT061.

Council of Science Editors:

Fruquiere A. Canaux calciques de type T spinaux et sensibilité douloureuse : Spinal T-type calcium channels and pain sensitivity. [Doctoral Dissertation]. Montpellier; 2018. Available from: http://www.theses.fr/2018MONTT061

Temple University

19. Jaleel, Naser. Re-Expression of T-Type Calcium Channels Minimally Affects Cardiac Contractility and Activates Pro-Survival Signaling Pathways in the Myocardium.

Degree: PhD, 2010, Temple University

URL: http://digital.library.temple.edu/u?/p245801coll10,83093

►

Physiology

The role of T-type calcium channels (TTCCs) in the heart is unclear. TTCCs are transiently expressed throughout the neonatal heart during a period of… (more)

▼

Physiology

The role of T-type calcium channels (TTCCs) in the heart is unclear. TTCCs are transiently expressed throughout the neonatal heart during a period of rapid cardiac development. A few weeks postnatally, TTCCs are no longer found in ventricular myocytes (VMs) and calcium influx via TTCCs (ICa,T) is only detected in the SA node and Purkinje system. However, pathologic cardiac stress is associated with re-expression of TTCCs in VMs. Whether ICa,T in this setting promotes cardiac growth or exacerbates cardiac function is a topic of debate. The focus of this thesis work was to examine the effect of TTCC re-expression in the normal and diseased myocardium. Our experiments were performed in a transgenic mouse model with inducible, cardiac-specific expression of α1G TTCCs. While both the α1G and α1H TTCC subtypes re-appear during cardiac disease, we specifically evaluated the effects of α1G TTCCs since mRNA levels of this TTCC subtype are markedly elevated during cardiac pathology. We found that transgenic mice with α1G overexpression had robust ICa,T with biophysical properties similar to those published in previous studies. α1G mice had a small increase in cardiac function and showed no evidence of cardiac histopathology or increased mortality. These findings were in contrast to the phenotype of transgenic mice with augmented L-type calcium channel (LTCC) activity secondary to overexpression of the β2a regulatory subunit. While the magnitude of calcium influx in α1G and β2a VMs was similar, we found that cardiac contractility of β2a mice was significantly greater than α1G mice. Also, β2a mice had significant cardiac fibrosis, myocyte death, and premature lethality compared to the benign phenotype of α1G mice. We showed that the phenotypic differences are likely related to the differential spatial localization of T- and LTCCs. Whereas α1G TTCCs were principally localized to the surface sarcolemma, LTCCs were primarily found in the transverse tubules in close proximity to the sites of sarcoplasmic reticulum calcium release. We evaluated the effect of TTCC expression during cardiac disease by inducing myocardial infarction (MI) in α1G mice. Acutely (1-week post MI), α1G mice showed similar worsening of cardiac function and mortality rates compared to control post-infarct mice. However, α1G hearts had smaller infarct sizes which correlated with increased Akt and NFAT activation in α1G than control hearts. After chronic heart failure, i.e. 7- weeks post-infarction, α1G hearts had significant hypertrophic response as determined by increased HW/BW ratio, myocyte cross-sectional area, as well as NFAT and Akt activity. Finally, α1G mice had a small survival benefit than control mice, which while statistically non-significant, suggests that TTCC re-expression does not exacerbate cardiac function as hypothesized by some investigators. We conclude that TTCCs play a minimal role in cardiac function and activate pro-survival signaling pathways in the myocardium.

Temple University – Theses

Advisors/Committee Members: Houser, Steven R., Autieri, Michael V., Eguchi, Satoru, Force, Thomas, Sabri, Abdelkarim.

Subjects/Keywords: Biology, Physiology; Biology, General; Cardiac Electrophysiology; Cardiac Hypertrophy; Excitation Contraction Coupling; L-Type Calcium Channels; T-type Calcium Channels

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

APA (6^th Edition):

Jaleel, N. (2010). Re-Expression of T-Type Calcium Channels Minimally Affects Cardiac Contractility and Activates Pro-Survival Signaling Pathways in the Myocardium. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,83093

Chicago Manual of Style (16^th Edition):

Jaleel, Naser. “Re-Expression of T-Type Calcium Channels Minimally Affects Cardiac Contractility and Activates Pro-Survival Signaling Pathways in the Myocardium.” 2010. Doctoral Dissertation, Temple University. Accessed April 18, 2021. http://digital.library.temple.edu/u?/p245801coll10,83093.

MLA Handbook (7^th Edition):

Jaleel, Naser. “Re-Expression of T-Type Calcium Channels Minimally Affects Cardiac Contractility and Activates Pro-Survival Signaling Pathways in the Myocardium.” 2010. Web. 18 Apr 2021.

Vancouver:

Jaleel N. Re-Expression of T-Type Calcium Channels Minimally Affects Cardiac Contractility and Activates Pro-Survival Signaling Pathways in the Myocardium. [Internet] [Doctoral dissertation]. Temple University; 2010. [cited 2021 Apr 18]. Available from: http://digital.library.temple.edu/u?/p245801coll10,83093.

Council of Science Editors:

Jaleel N. Re-Expression of T-Type Calcium Channels Minimally Affects Cardiac Contractility and Activates Pro-Survival Signaling Pathways in the Myocardium. [Doctoral Dissertation]. Temple University; 2010. Available from: http://digital.library.temple.edu/u?/p245801coll10,83093

20. Stephens, Robert. The Role of Domain II and Domain IV Extracellular Turrets in Determining Ion Selectivity in the T-type Calcium Channel from Lymnaea stagnalis.

Degree: 2016, University of Waterloo

URL: http://hdl.handle.net/10012/10590

► The T-type calcium channel from the pond snail Lymnaea stagnalis, LCav3, undergoes alternative splicing in exon 12. Exon 12 codes for the L5 structure (S5-P)… (more)

Subjects/Keywords: Calcium Channels; T-type Calcium Channel; Giant Pond Snail; Electrophysiology; Membrane Biophysics; Ion Selectivity; Ion Permeability; Calcium Permeability; Sodium Permeability

…11 Figure 1.4 Structure of the Voltage-gated T-type Calcium Channel… …gated channel (HCN), and L- and T- type channel calcium currents (Grant, 2009… …the presence of two splice isoforms of the T-type calcium channel from Lymnaea stagnalis… …Domain II and Domain IV in determining ion selectivity in the T-type calcium channel from L… …Structure of the Voltage-gated T-type Calcium Channel The structure of the T-type calcium channel…

11 more images…

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APA (6^th Edition):

Stephens, R. (2016). The Role of Domain II and Domain IV Extracellular Turrets in Determining Ion Selectivity in the T-type Calcium Channel from Lymnaea stagnalis. (Thesis). University of Waterloo. Retrieved from http://hdl.handle.net/10012/10590

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):

Stephens, Robert. “The Role of Domain II and Domain IV Extracellular Turrets in Determining Ion Selectivity in the T-type Calcium Channel from Lymnaea stagnalis.” 2016. Thesis, University of Waterloo. Accessed April 18, 2021. http://hdl.handle.net/10012/10590.

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

MLA Handbook (7^th Edition):

Stephens, Robert. “The Role of Domain II and Domain IV Extracellular Turrets in Determining Ion Selectivity in the T-type Calcium Channel from Lymnaea stagnalis.” 2016. Web. 18 Apr 2021.

Vancouver:

Stephens R. The Role of Domain II and Domain IV Extracellular Turrets in Determining Ion Selectivity in the T-type Calcium Channel from Lymnaea stagnalis. [Internet] [Thesis]. University of Waterloo; 2016. [cited 2021 Apr 18]. Available from: http://hdl.handle.net/10012/10590.

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

Council of Science Editors:

Stephens R. The Role of Domain II and Domain IV Extracellular Turrets in Determining Ion Selectivity in the T-type Calcium Channel from Lymnaea stagnalis. [Thesis]. University of Waterloo; 2016. Available from: http://hdl.handle.net/10012/10590

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

University of Toledo

21. Zahratka, Jeffrey Allen. Serotonin Modulates a Calcium-Driven Negative Feedback Loop in a C. elegans Nociceptor.

Degree: PhD, Biology (Cell-Molecular Biology), 2015, University of Toledo

URL: http://rave.ohiolink.edu/etdc/view?acc_num=toledo1449748910

► Neuromodulation in sensory circuits is critical because it allows an organism to respond appropriately to a given stimulus. Sensory systems are modulated by monoamine… (more)

Subjects/Keywords: Biology; Neurobiology; Neurosciences; Caenorhabditis elegans; C elegans; ASH; neuromodulation; serotonin; 5-HT; calcium; calcium channel; calcium imaging; electrophysiology; neuropeptide; nociception; L-type channel; G-protein coupled receptor; GPCR

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APA (6^th Edition):

Zahratka, J. A. (2015). Serotonin Modulates a Calcium-Driven Negative Feedback Loop in a C. elegans Nociceptor. (Doctoral Dissertation). University of Toledo. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=toledo1449748910

Chicago Manual of Style (16^th Edition):

Zahratka, Jeffrey Allen. “Serotonin Modulates a Calcium-Driven Negative Feedback Loop in a C. elegans Nociceptor.” 2015. Doctoral Dissertation, University of Toledo. Accessed April 18, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1449748910.

MLA Handbook (7^th Edition):

Zahratka, Jeffrey Allen. “Serotonin Modulates a Calcium-Driven Negative Feedback Loop in a C. elegans Nociceptor.” 2015. Web. 18 Apr 2021.

Vancouver:

Zahratka JA. Serotonin Modulates a Calcium-Driven Negative Feedback Loop in a C. elegans Nociceptor. [Internet] [Doctoral dissertation]. University of Toledo; 2015. [cited 2021 Apr 18]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=toledo1449748910.

Council of Science Editors:

Zahratka JA. Serotonin Modulates a Calcium-Driven Negative Feedback Loop in a C. elegans Nociceptor. [Doctoral Dissertation]. University of Toledo; 2015. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=toledo1449748910

University of Toronto

22. Korogyi, Adam S. Mechanisms of Atrial Fibrillation in Mice with Genetic Ablation of the α1D L-type Calcium Channel.

Degree: 2014, University of Toronto

URL: http://hdl.handle.net/1807/71517

►

Atrial fibrillation (AF) is the most common supraventricular arrhythmia with a multifactorial pathophysiology. Reductions in α1 L-type calcium channel (LTCC) current (ICaL) and action potential… (more)

Subjects/Keywords: atrial fibrillation; cav1.3; arrhythmia; atria; alternans; electrophysiology; heart; L-type calcium channel; 0719

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APA (6^th Edition):

Korogyi, A. S. (2014). Mechanisms of Atrial Fibrillation in Mice with Genetic Ablation of the α1D L-type Calcium Channel. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/71517

Chicago Manual of Style (16^th Edition):

Korogyi, Adam S. “Mechanisms of Atrial Fibrillation in Mice with Genetic Ablation of the α1D L-type Calcium Channel.” 2014. Masters Thesis, University of Toronto. Accessed April 18, 2021. http://hdl.handle.net/1807/71517.

MLA Handbook (7^th Edition):

Korogyi, Adam S. “Mechanisms of Atrial Fibrillation in Mice with Genetic Ablation of the α1D L-type Calcium Channel.” 2014. Web. 18 Apr 2021.

Vancouver:

Korogyi AS. Mechanisms of Atrial Fibrillation in Mice with Genetic Ablation of the α1D L-type Calcium Channel. [Internet] [Masters thesis]. University of Toronto; 2014. [cited 2021 Apr 18]. Available from: http://hdl.handle.net/1807/71517.

Council of Science Editors:

Korogyi AS. Mechanisms of Atrial Fibrillation in Mice with Genetic Ablation of the α1D L-type Calcium Channel. [Masters Thesis]. University of Toronto; 2014. Available from: http://hdl.handle.net/1807/71517

University of Toronto

23. Rozanski, Gabriela Maria. The Sandwich Synapse: Trans-glial Signaling Between Neuronal Somata in the Dorsal Root Ganglion.

Degree: PhD, 2014, University of Toronto

URL: http://hdl.handle.net/1807/73784

► The dorsal root ganglion (DRG) contains the cell bodies of primary somatosensory neurons that form axonal connections for the transfer of sensory input from the… (more)

Subjects/Keywords: dorsal root ganglion; glutamatergic; patch clamp; purinergic; trans-glial; T-type channel; 0317

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APA (6^th Edition):

Rozanski, G. M. (2014). The Sandwich Synapse: Trans-glial Signaling Between Neuronal Somata in the Dorsal Root Ganglion. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/73784

Chicago Manual of Style (16^th Edition):

Rozanski, Gabriela Maria. “The Sandwich Synapse: Trans-glial Signaling Between Neuronal Somata in the Dorsal Root Ganglion.” 2014. Doctoral Dissertation, University of Toronto. Accessed April 18, 2021. http://hdl.handle.net/1807/73784.

MLA Handbook (7^th Edition):

Rozanski, Gabriela Maria. “The Sandwich Synapse: Trans-glial Signaling Between Neuronal Somata in the Dorsal Root Ganglion.” 2014. Web. 18 Apr 2021.

Vancouver:

Rozanski GM. The Sandwich Synapse: Trans-glial Signaling Between Neuronal Somata in the Dorsal Root Ganglion. [Internet] [Doctoral dissertation]. University of Toronto; 2014. [cited 2021 Apr 18]. Available from: http://hdl.handle.net/1807/73784.

Council of Science Editors:

Rozanski GM. The Sandwich Synapse: Trans-glial Signaling Between Neuronal Somata in the Dorsal Root Ganglion. [Doctoral Dissertation]. University of Toronto; 2014. Available from: http://hdl.handle.net/1807/73784

Université de Sherbrooke

24. Savard, Alexandre. Caractérisation de la protéine Gimap5 chez les lymphocytes T.

Degree: 2011, Université de Sherbrooke

URL: http://savoirs.usherbrooke.ca/handle/11143/4070

► Le diabète de Type 1 est une maladie auto-immune caractérisée par la perte de production d'insuline par les îlots [béta] du pancréas. Les causes menant… (more)

▼ Le diabète de Type 1 est une maladie auto-immune caractérisée par la perte de production d'insuline par les îlots [béta] du pancréas. Les causes menant à la destruction de ces îlots par les cellules T autoréactives sont méconnues. Certains événements tels qu'une infection virale ou des facteurs environnementaux peuvent déclencher cette auto-immunité. Chez le rat BB-DP qui développe un diabète de type 1 semblable à l'homme, une mutation qui affecte les cellules T a été découverte. La mutation nommée lyp amène une perte de survie des cellules T dans la périphérie malgré tous les facteurs de survie des cellules T présents chez l'animal. Cette mutation située sur le chromosome 4 affecte un gène de la famille GIMAP, plus particulièrement la protéine GIMAP5 qui se retrouve tronquée et non fonctionnelle. Des résultats du laboratoire ont démontré une implication de GIMAP5 dans la voie du calcium. La manière par laquelle GIMAP5 joue son rôle dans la survie des lymphocytes T n'est pas connue. Afin de comprendre ces fonctions, nous voulons identifier la localisation cellulaire de GIMAP5 ainsi que ses partenaires d'interaction. Les lignées cellulaires transfectées avec le gène de GIMAP5 étiqueté ont été marquées en fluorescence à l'aide de marqueurs d'organelles et examinées en microscopie confocale afin de déterminer la localisation de GIMAP5. Une étude de double-hybride combinée avec des marquages fluorescents à l'aide d'anticorps fluorescents dirigés contre ces protéines et l'utilisation de la microscopie confocale permettent de vérifier les partenaires d'interaction de GIMAP5. Les cellules T de rats gimap5[indice supérieur lyp/lyp] et sauvages ont été utilisées afin de faire des marquages au Rhod-2 (calcium mitochondrial) et de vérifier l'effet de la mutation sur la capacité des mitochondries à absorber le calcium. Une localisation de GIMAP5 au niveau du RE a été identifiée dans les cellules HEK 293T surexprimant GIMAP5, mais n'as [i.e. n'a] pu être vu chez les lignées de cellules T Jurkats. Les résultats de l'étude de double-hybride ont donné des partenaires d'interaction de faible affinité (avec une cote de D). Les essais de microscopie confocale n'ont pu démontrer cette interaction. Finalement, les mitochondries des cellules T de rats gimap5[indice supérieur lyp/lyp] ont une vitesse d'incorporation du calcium plus lente et un retour à la normale plus lent que les mitochondries des cellules T de rats sauvages. Chez le rat, GIMAP5 semble jouer un rôle au niveau de l'homéostasie du calcium et de l'intégrité des mitochondries, puisque la mutation gimap5[indice supérieur lyp/lyp] apporte une baisse du potentiel membranaire des mitochondries et une baisse de l'accumulation du calcium par ces dernières.Le mécanisme par lequel GIMAP5 régule l'homéostasie du calcium reste encore à élucider. Advisors/Committee Members: Ramanathan, Sheela (advisor), Ilangumaran, Subburaj (advisor).

Subjects/Keywords: Auto-immunité; Diabète de type 1; Homéostasie; Calcium; Survie; Lymphocytes T; GIMAP5

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APA (6^th Edition):

Savard, A. (2011). Caractérisation de la protéine Gimap5 chez les lymphocytes T. (Masters Thesis). Université de Sherbrooke. Retrieved from http://savoirs.usherbrooke.ca/handle/11143/4070

Chicago Manual of Style (16^th Edition):

Savard, Alexandre. “Caractérisation de la protéine Gimap5 chez les lymphocytes T.” 2011. Masters Thesis, Université de Sherbrooke. Accessed April 18, 2021. http://savoirs.usherbrooke.ca/handle/11143/4070.

MLA Handbook (7^th Edition):

Savard, Alexandre. “Caractérisation de la protéine Gimap5 chez les lymphocytes T.” 2011. Web. 18 Apr 2021.

Vancouver:

Savard A. Caractérisation de la protéine Gimap5 chez les lymphocytes T. [Internet] [Masters thesis]. Université de Sherbrooke; 2011. [cited 2021 Apr 18]. Available from: http://savoirs.usherbrooke.ca/handle/11143/4070.

Council of Science Editors:

Savard A. Caractérisation de la protéine Gimap5 chez les lymphocytes T. [Masters Thesis]. Université de Sherbrooke; 2011. Available from: http://savoirs.usherbrooke.ca/handle/11143/4070

University of Melbourne

25. ALI, IDRISH. Enduring electrophysiological effects of early life stress in brain: implications for limbic epilepsy.

Degree: 2013, University of Melbourne

URL: http://hdl.handle.net/11343/38021

► Introduction: In both humans and in animal models, stress during early life has been reported to have adverse consequences for various neuropsychiatric disorders in adulthood,… (more)

▼ Introduction: In both humans and in animal models, stress during early life has been reported to have adverse consequences for various neuropsychiatric disorders in adulthood, including mood and anxiety disorders and cognitive impairment. In addition, early-life stress (ELS) has also been shown to lead to an enduring vulnerability to amygdala kindling-induced epileptogenesis in rats, an important model of human mesial temporal lobe epilepsy (MTLE). Although a range of neuroplastic, neuroendocrine and neurochemical approaches have been employed to determine the underlying mechanisms, there has been little investigation in to the electrophysiological mechanisms. Electrophysiological methods investigating changes in neuronal firing patterns in the circuits relevant to epileptogenesis and stress biology can help shed light on downstream outcomes of other ELS-induced neurobiological effects. Key structures include the hippocampus, which is not only highly implicated in MTLE but also is critical in stress biology; in addition, recent studies suggest involvement of thalamocortical circuits in the progression of kindling. Hence this study investigated the effects in rats of ELS and amygdala kindling on in vivo neuronal firing patterns in the hippocampus, as well as in thalamic and cortical regions. Methods: Eight week old male Wistar rats, previously exposed to maternal separation (MS) induced ELS or early handling (EH), underwent amygdala kindling (or sham kindling). This involved delivering two electrical stimulations per day via a bipolar electrode implanted in the basolateral amygdala, until the rats were fully kindled (five class V seizures; Racine’s scale (1972)). Once fully kindled, in vivo juxtacellular recordings in key hippocampal, thalamic and cortical regions were performed under neuroleptic analgesia. Molecular mechanisms potentially associated with the electrophysiological changes, including mRNA expression of T-type calcium channels and voltage-gated sodium channels, were investigated using quantitative real-time polymerase chain reaction (qPCR). Results: In the thalamic reticular nucleus (TRN) both kindling and MS independently lowered neuronal firing frequency and enhanced the percentage of action potentials firing in bursts during interictal periods. Further, TRN burst firing was significantly increased in kindled MS rats, when compared to kindled EH rats. In addition, MS enhanced the percentage of action potentials firing in bursts in hippocampal pyramidal neurons. Following a stimulation-induced limbic seizure, there was a significant increase in the neuronal firing frequency and burst firing of somatosensory cortex, and neuronal firing frequency of the TRN. Importantly, somatosensory cortical neurons exhibited a more pronounced increase in percentage of burst firing in MS rats than in EH rats. A reduced expression of voltage-gated sodium channel mRNA expression was…

Subjects/Keywords: early life stress; neuronal firing; limbic epilepsy; thalamic reticular nucleus; hippocampus; T-type calcium channels

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APA (6^th Edition):

ALI, I. (2013). Enduring electrophysiological effects of early life stress in brain: implications for limbic epilepsy. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/38021

Chicago Manual of Style (16^th Edition):

ALI, IDRISH. “Enduring electrophysiological effects of early life stress in brain: implications for limbic epilepsy.” 2013. Doctoral Dissertation, University of Melbourne. Accessed April 18, 2021. http://hdl.handle.net/11343/38021.

MLA Handbook (7^th Edition):

ALI, IDRISH. “Enduring electrophysiological effects of early life stress in brain: implications for limbic epilepsy.” 2013. Web. 18 Apr 2021.

Vancouver:

ALI I. Enduring electrophysiological effects of early life stress in brain: implications for limbic epilepsy. [Internet] [Doctoral dissertation]. University of Melbourne; 2013. [cited 2021 Apr 18]. Available from: http://hdl.handle.net/11343/38021.

Council of Science Editors:

ALI I. Enduring electrophysiological effects of early life stress in brain: implications for limbic epilepsy. [Doctoral Dissertation]. University of Melbourne; 2013. Available from: http://hdl.handle.net/11343/38021

University of Alberta

26. Soliman, Daniel. Ion transport pharmacology in heart disease and type-2 diabetes.

Degree: PhD, Department of Pharmacology, 2010, University of Alberta

URL: https://era.library.ualberta.ca/files/0c483j64n

► The cardiac sodium-calcium exchanger (NCX) is an important membrane protein which regulates cellular calcium necessary for the optimal contractile function of the heart. NCX has… (more)

▼ The cardiac sodium-calcium exchanger (NCX) is an important membrane protein which regulates cellular calcium necessary for the optimal contractile function of the heart. NCX has become a focal point in ischemic heart disease (IHD) research as evidence suggests that reactive oxygen species (ROS) produced during IHD can cause NCX to malfunction resulting in an intracellular calcium overload leading to cardiac contractile abnormalities. Therefore, I hypothesized that NCX function is mediated by ROS increasing NCX1 activity during cardiac ischemia-reperfusion. To research this hypothesis, I investigated cellular mechanisms which may play a role in NCX dysfunction and also examined methods to correct NCX function. I found that reactive oxygen species directly and irreversibly modify NCX protein, increasing its activity, thereby worsening the calcium overload which is deleterious to cardiac function. I also elucidated the molecular means by which NCX protein modification occurs. Exploring pharmacological means by which to decrease NCX function to relieve the calcium overload and reduce the damage to the heart, I discovered that ranolazine (Ranexa™), indicated for the treatment of angina pectoris inhibits NCX activity directly, thereby further reducing the calcium overload-induced injury to the heart. Furthermore, many IHD patients are also co-morbid for type-2 diabetes. These patients are prescribed sulfonylurea (SU) agents which act at the ATP sensitive K+ channel (KATP). One agent such as glibenclamide is known to have cardiotoxic side effects. Therefore, SUs devoid of any cardiac side effects would beneficial. Interestingly, patients possessing the genetic variant E23K-S1369A KATP channel have improved blood glucose levels with the use of the SU gliclazide. Therefore, I determined the functional mechanism by which gliclazide has increased inhibition at the KATP channel. These findings have implications for type-2 diabetes therapy, in which 20% of the type-2 diabetic population carries the KATP channel variant. In summary, the findings presented in this thesis have implications on treatment strategies in the clinical setting, as a NCX inhibitor can be beneficial in IHD and possibly type-2 diabetes. Moreover, a pharmacogenomic approach in treating type-2 diabetes may also provide a positive outcome when considering co-morbid cardiac complications such as atrial fibrillation and heart failure.

Subjects/Keywords: type-2 diabetes; ATP-sensitive potassium channel; ranolazine; sodium-calcium exchanger; heart disease; pharmacology; sulfonylureas; reactive oxygen species; patch clamping

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APA (6^th Edition):

Soliman, D. (2010). Ion transport pharmacology in heart disease and type-2 diabetes. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/0c483j64n

Chicago Manual of Style (16^th Edition):

Soliman, Daniel. “Ion transport pharmacology in heart disease and type-2 diabetes.” 2010. Doctoral Dissertation, University of Alberta. Accessed April 18, 2021. https://era.library.ualberta.ca/files/0c483j64n.

MLA Handbook (7^th Edition):

Soliman, Daniel. “Ion transport pharmacology in heart disease and type-2 diabetes.” 2010. Web. 18 Apr 2021.

Vancouver:

Soliman D. Ion transport pharmacology in heart disease and type-2 diabetes. [Internet] [Doctoral dissertation]. University of Alberta; 2010. [cited 2021 Apr 18]. Available from: https://era.library.ualberta.ca/files/0c483j64n.

Council of Science Editors:

Soliman D. Ion transport pharmacology in heart disease and type-2 diabetes. [Doctoral Dissertation]. University of Alberta; 2010. Available from: https://era.library.ualberta.ca/files/0c483j64n

27. 김, 민지. Regulation od the N-Type calcium channel gene by C/EBP.

Degree: 2001, Ajou University

URL: http://repository.ajou.ac.kr/handle/201003/2209 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000008205

Master Advisors/Committee Members: 대학원 의학과, 199924311, 김, 민지.

Subjects/Keywords: C/EBP; N-Type; calcium; channel; gene

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APA (6^th Edition):

김, �. (2001). Regulation od the N-Type calcium channel gene by C/EBP. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/2209 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000008205

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):

김, 민지. “Regulation od the N-Type calcium channel gene by C/EBP.” 2001. Thesis, Ajou University. Accessed April 18, 2021. http://repository.ajou.ac.kr/handle/201003/2209 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000008205.

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

MLA Handbook (7^th Edition):

김, 민지. “Regulation od the N-Type calcium channel gene by C/EBP.” 2001. Web. 18 Apr 2021.

Vancouver:

김 �. Regulation od the N-Type calcium channel gene by C/EBP. [Internet] [Thesis]. Ajou University; 2001. [cited 2021 Apr 18]. Available from: http://repository.ajou.ac.kr/handle/201003/2209 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000008205.

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

Council of Science Editors:

김 �. Regulation od the N-Type calcium channel gene by C/EBP. [Thesis]. Ajou University; 2001. Available from: http://repository.ajou.ac.kr/handle/201003/2209 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000008205

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

University of Colorado

28. Chapman, Timothy Ross. Interactions of Aging, Inflammation, and Neuronal Function: Synaptic Plasticity in Older Rodents is Altered Following a Peripheral Immune Challenge.

Degree: PhD, Psychology & Neuroscience, 2013, University of Colorado

URL: https://scholar.colorado.edu/psyc_gradetds/44

► It is well accepted that early stages of cognitive decline and memory loss involve altered synaptic plasticity in the hippocampus and related structures. It… (more)

▼ It is well accepted that early stages of cognitive decline and memory loss involve altered synaptic plasticity in the hippocampus and related structures. It has been proposed that calcium homeostasis in principal neurons of the hippocampus becomes `dysregulated' with age. Specifically, a decline in N-methyl-D-aspartate receptors (NMDA receptors) and an increase in L-type voltage-dependent calcium channels may reduce overall neuronal excitability and synaptic plasticity. This is believed to shift synaptic plasticity in the aged brain away from long-term potentiation (LTP) and toward long-term depression (LTD). Another major change that occurs with age is increased brain inflammation. It has been demonstrated in aged rodents that a peripheral immune challenge with Escherichia coli triggers a prolonged inflammatory response in the hippocampus, which impairs long-term memory consolidation in the days following. Because this process is dependent upon synaptic plasticity in region CA1 of the hippocampus, we explored LTP and LTD there as well changes in NMDA receptors and L- type calcium channels. We found that a peripheral infection in aged rats decreases LTP following theta-burst stimulation but increases LTD following low frequency stimulations, both of which are dependent upon NMDA receptors. However, infection decreases a more robust LTP following high frequency stimulation in young rats, and reduces the contribution of L-type calcium channels in both young and aged rats. These effects are not associated with major changes in NMDA receptors or L-type calcium channels in the synapse, and only the GluN2B subunit of NMDA receptor is significantly increased. Inflammation has been demonstrated to increase neural excitability, yet the overall effect of inflammation in our studies was reduced LTP and enhanced LTD. It is therefore possible that some of the changes in calcium homeostasis and synaptic plasticity that occur with age are either caused by or activated as a neuroprotective mechanism against increased inflammation. Advisors/Committee Members: Susan L. Patterson, Steve F. Maier, Jerry W. Rudy, Robert L. Spencer, Gregory Carey.

Subjects/Keywords: long term depression; long term potentiation; L-type calcium channel; metaplasticity; NMDA receptor; Synaptic Plasticity; Neuroscience and Neurobiology

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APA (6^th Edition):

Chapman, T. R. (2013). Interactions of Aging, Inflammation, and Neuronal Function: Synaptic Plasticity in Older Rodents is Altered Following a Peripheral Immune Challenge. (Doctoral Dissertation). University of Colorado. Retrieved from https://scholar.colorado.edu/psyc_gradetds/44

Chicago Manual of Style (16^th Edition):

Chapman, Timothy Ross. “Interactions of Aging, Inflammation, and Neuronal Function: Synaptic Plasticity in Older Rodents is Altered Following a Peripheral Immune Challenge.” 2013. Doctoral Dissertation, University of Colorado. Accessed April 18, 2021. https://scholar.colorado.edu/psyc_gradetds/44.

MLA Handbook (7^th Edition):

Chapman, Timothy Ross. “Interactions of Aging, Inflammation, and Neuronal Function: Synaptic Plasticity in Older Rodents is Altered Following a Peripheral Immune Challenge.” 2013. Web. 18 Apr 2021.

Vancouver:

Chapman TR. Interactions of Aging, Inflammation, and Neuronal Function: Synaptic Plasticity in Older Rodents is Altered Following a Peripheral Immune Challenge. [Internet] [Doctoral dissertation]. University of Colorado; 2013. [cited 2021 Apr 18]. Available from: https://scholar.colorado.edu/psyc_gradetds/44.

Council of Science Editors:

Chapman TR. Interactions of Aging, Inflammation, and Neuronal Function: Synaptic Plasticity in Older Rodents is Altered Following a Peripheral Immune Challenge. [Doctoral Dissertation]. University of Colorado; 2013. Available from: https://scholar.colorado.edu/psyc_gradetds/44

29. Blazon, Maxwell Robert. REGULATION OF GABA RELEASE BY PRESYNAPTIC CAV2.2 IN THE BASOLATERAL AMYGDALA AND INFRALIMBIC CORTEX.

Degree: MS, 2018, University of New Hampshire

URL: https://scholars.unh.edu/thesis/1178

► Anxiety is linked to dysregulation of neuronal activity in several brain regions including the infralimbic (IL) area of the medial prefrontal cortex (mPFC) and the… (more)

▼ Anxiety is linked to dysregulation of neuronal activity in several brain regions including the infralimbic (IL) area of the medial prefrontal cortex (mPFC) and the basolateral nucleus of the amygdala (BLA). Disruptions to the balance of excitatory and inhibitory signaling in these regions are implicated in anxiety-like behaviors in animals and anxiety disorders in humans. The neuronal circuitry between excitatory neurons, known as pyramidal cells (P-cells), and inhibitory neurons, known as interneurons (INs), is a primary target for anxiety modulation at the cellular level. INs, particularly the subtype that contain the neuropeptide cholecystokinin (CCK+INs), form inhibitory synapses around P-cells. Through GABAergic neurotransmitter release, CCK+INs regulate P-cell activity and subsequent anxiety-related neuronal output. Two protein complexes, the N-type calcium channel (CaV2.2) and the type-1 cannabinoid receptor (CB1), are expressed in the presynaptic terminal of CCK+INs. CaV2.2 and CB1 have been shown to regulate neurotransmitter release from CCK+INs in the hippocampus, but it is not known if this role is conserved in the anxiety-related neuronal circuits of the BLA and IL. CaV2.2 has also been shown to regulate the intrinsic firing properties of P-cells in the hippocampus and deep cerebellar nuclei, but this role has not been demonstrated in the IL. To investigate these neuronal circuits, I used a combination of transgenic mouse models, confocal microscopy, patch-clamp electrophysiology, optogenetics, and pharmacology. In the first chapter of my thesis, I investigated the role of CaV2.2 in CCK+IN/P-cell synapses in the BLA. In the second chapter of my thesis, I investigated the role of CB1 in regulating GABA release from CCK+INs in the BLA. In the third chapter of my thesis, I assessed the regulation of GABA release and intrinsic firing by CaV2.2 in the IL. I present electrophysiology data which demonstrate GABA release from CCK+INs is partially CaV2.2-dependent in the BLA. I obtained preliminary electrophysiology recordings which suggest CB1 receptors modulate GABA release in CCK+IN/P-cell synapses in the BLA. I found that neurotransmitter release from GABAergic INs is partially CaV2.2-dependent in the IL. I found that GABA release from CCK+INs is not CaV2.2-dependent in this region. Lastly, I observed that CaV2.2 plays a minimal role in the intrinsic firing properties of P-cells in the IL. My findings suggest that CaV2.2 differentially regulates GABA release and intrinsic firing properties across brain regions, suggesting there are region-specific implications of CaV2.2 modulation in anxiety-related neuronal output. Advisors/Committee Members: Arturo A Andrade, Win H Watson, Jill A McGaughy.

Subjects/Keywords: Anxiety; Basolateral Amygdala; Cholecystokinin (CCK)-Containing Interneurons; Infralimbic Cortex; Neurotransmitter Release; N-type Calcium Channel (CaV2.2); Pharmacology; Molecular biology; Neurosciences

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APA (6^th Edition):

Blazon, M. R. (2018). REGULATION OF GABA RELEASE BY PRESYNAPTIC CAV2.2 IN THE BASOLATERAL AMYGDALA AND INFRALIMBIC CORTEX. (Thesis). University of New Hampshire. Retrieved from https://scholars.unh.edu/thesis/1178

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):

Blazon, Maxwell Robert. “REGULATION OF GABA RELEASE BY PRESYNAPTIC CAV2.2 IN THE BASOLATERAL AMYGDALA AND INFRALIMBIC CORTEX.” 2018. Thesis, University of New Hampshire. Accessed April 18, 2021. https://scholars.unh.edu/thesis/1178.

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

MLA Handbook (7^th Edition):

Blazon, Maxwell Robert. “REGULATION OF GABA RELEASE BY PRESYNAPTIC CAV2.2 IN THE BASOLATERAL AMYGDALA AND INFRALIMBIC CORTEX.” 2018. Web. 18 Apr 2021.

Vancouver:

Blazon MR. REGULATION OF GABA RELEASE BY PRESYNAPTIC CAV2.2 IN THE BASOLATERAL AMYGDALA AND INFRALIMBIC CORTEX. [Internet] [Thesis]. University of New Hampshire; 2018. [cited 2021 Apr 18]. Available from: https://scholars.unh.edu/thesis/1178.

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

Council of Science Editors:

Blazon MR. REGULATION OF GABA RELEASE BY PRESYNAPTIC CAV2.2 IN THE BASOLATERAL AMYGDALA AND INFRALIMBIC CORTEX. [Thesis]. University of New Hampshire; 2018. Available from: https://scholars.unh.edu/thesis/1178

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

Colorado State University

30. Chaplin, Nathan L. Oxidant-dependent regulation of L-type calcium channel activity by angiotensin in vascular smooth muscle.

Degree: PhD, Biomedical Sciences, 2015, Colorado State University

URL: http://hdl.handle.net/10217/170373

► Resistance arteries are a major point of physiological regulation of blood flow. Increases in vessel wall stress or sympathetic activity stimulate vascular wall angiotensin signaling,… (more)

▼ Resistance arteries are a major point of physiological regulation of blood flow. Increases in vessel wall stress or sympathetic activity stimulate vascular wall angiotensin signaling, resulting in smooth muscle contraction which directly increases peripheral resistance. Calcium influx through voltage-gated L-type calcium channels underlies vascular smooth muscle contraction. Roughly half of calcium influx in these cells occurs through a small number of persistently active channels, whose activity increases with membrane depolarization. The number of channels gating in this manner is increased by activation of angiotensin receptors on the cell membrane, and basal L-type channel activity is increased during hypertension. Reactive oxygen species are also generated by vascular smooth muscle in response to vessel stretch and by several paracrine signaling pathways including angiotensin signaling. Oxidative stress and augmented calcium handling resulting from chronic angiotensin signaling in the vasculature each contribute to enhanced vessel reactivity, pathological inflammation and vessel remodeling associated with hypertension. This study uses a multidisciplinary approach to investigate the role of hydrogen peroxide in angiotensin signaling in vascular smooth muscle. Using calcium- and redox-sensitive fluorescent indicators, local generation of hydrogen peroxide by NAD(P)H oxidase and mitochondria are shown to synergistically promote PKC-dependent persistent gating of plasma membrane L- type calcium channels in response to angiotensin II. We show that broad inhibition of hydrogen peroxide signaling by catalase and targeted inhibition of mitochondrial reactive oxygen species production attenuates cerebral resistance artery constriction to angiotensin. We further demonstrate the role of endothelium-independent mitochondrial reactive oxygen species in development of enhanced vessel tone and smooth muscle calcium in a murine model of hypertension. Together, these findings contribute to the understanding of intracellular calcium and oxidative signaling in vascular physiology and disease and may provide insight into local signaling dynamics involving these second messengers in various other systems. Advisors/Committee Members: Amberg, Gregory (advisor), DeLuca, Jennifer (committee member), Tamkun, Michael (committee member), Tsunoda, Susan (committee member).

Subjects/Keywords: angiotensin; L-type calcium channel; mitochondria; NAD(P)H oxidase; reactive oxygen species; vascular smooth muscle

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APA (6^th Edition):

Chaplin, N. L. (2015). Oxidant-dependent regulation of L-type calcium channel activity by angiotensin in vascular smooth muscle. (Doctoral Dissertation). Colorado State University. Retrieved from http://hdl.handle.net/10217/170373

Chicago Manual of Style (16^th Edition):

Chaplin, Nathan L. “Oxidant-dependent regulation of L-type calcium channel activity by angiotensin in vascular smooth muscle.” 2015. Doctoral Dissertation, Colorado State University. Accessed April 18, 2021. http://hdl.handle.net/10217/170373.

MLA Handbook (7^th Edition):

Chaplin, Nathan L. “Oxidant-dependent regulation of L-type calcium channel activity by angiotensin in vascular smooth muscle.” 2015. Web. 18 Apr 2021.

Vancouver:

Chaplin NL. Oxidant-dependent regulation of L-type calcium channel activity by angiotensin in vascular smooth muscle. [Internet] [Doctoral dissertation]. Colorado State University; 2015. [cited 2021 Apr 18]. Available from: http://hdl.handle.net/10217/170373.

Council of Science Editors:

Chaplin NL. Oxidant-dependent regulation of L-type calcium channel activity by angiotensin in vascular smooth muscle. [Doctoral Dissertation]. Colorado State University; 2015. Available from: http://hdl.handle.net/10217/170373

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