subject:(Oligodendroglia)

Universidad Autónoma de Madrid

1. Fasciani, Ilaria. Caracterización electrofisiológica de los canales de Cx47 oligodendrocitarios y del sincitio panglial: Efecto de las mutaciones asociadas a leucodistrofia hipomielinizante(enfermedad de Pelizaeus-Merzbacher) .

Degree: 2014, Universidad Autónoma de Madrid

URL: http://hdl.handle.net/10486/660260

Subjects/Keywords: Oligodendroglia - Tesis doctorales

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APA (6^th Edition):

Fasciani, I. (2014). Caracterización electrofisiológica de los canales de Cx47 oligodendrocitarios y del sincitio panglial: Efecto de las mutaciones asociadas a leucodistrofia hipomielinizante(enfermedad de Pelizaeus-Merzbacher) . (Doctoral Dissertation). Universidad Autónoma de Madrid. Retrieved from http://hdl.handle.net/10486/660260

Chicago Manual of Style (16^th Edition):

Fasciani, Ilaria. “Caracterización electrofisiológica de los canales de Cx47 oligodendrocitarios y del sincitio panglial: Efecto de las mutaciones asociadas a leucodistrofia hipomielinizante(enfermedad de Pelizaeus-Merzbacher) .” 2014. Doctoral Dissertation, Universidad Autónoma de Madrid. Accessed January 20, 2021. http://hdl.handle.net/10486/660260.

MLA Handbook (7^th Edition):

Fasciani, Ilaria. “Caracterización electrofisiológica de los canales de Cx47 oligodendrocitarios y del sincitio panglial: Efecto de las mutaciones asociadas a leucodistrofia hipomielinizante(enfermedad de Pelizaeus-Merzbacher) .” 2014. Web. 20 Jan 2021.

Vancouver:

Fasciani I. Caracterización electrofisiológica de los canales de Cx47 oligodendrocitarios y del sincitio panglial: Efecto de las mutaciones asociadas a leucodistrofia hipomielinizante(enfermedad de Pelizaeus-Merzbacher) . [Internet] [Doctoral dissertation]. Universidad Autónoma de Madrid; 2014. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/10486/660260.

Council of Science Editors:

Fasciani I. Caracterización electrofisiológica de los canales de Cx47 oligodendrocitarios y del sincitio panglial: Efecto de las mutaciones asociadas a leucodistrofia hipomielinizante(enfermedad de Pelizaeus-Merzbacher) . [Doctoral Dissertation]. Universidad Autónoma de Madrid; 2014. Available from: http://hdl.handle.net/10486/660260

Universidade do Estado do Rio de Janeiro

2. Tiago Savignon Cardoso Machado. Efeitos de lesão por hipóxia-isquemia pré-natal sobre o desenvolvimento do sistema motor: córtex e cerebelo.

Degree: Master, 2008, Universidade do Estado do Rio de Janeiro

URL: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=2067 ;

► Crianças que sofrem insultos hipóxico-isquêmicos perinatais têm hipomielinização, astrogliose e desenvolvimento cortical alterado. Robinson e cols., usando um modelo de hipóxia-isquemia (HI) por obstrução das… (more)

▼ Crianças que sofrem insultos hipóxico-isquêmicos perinatais têm hipomielinização, astrogliose e desenvolvimento cortical alterado. Robinson e cols., usando um modelo de hipóxia-isquemia (HI) por obstrução das artérias uterinas na rata grávida, mostraram astrogliose, morte de oligodendrócitos e ruptura axonal na prole. Neste trabalho avaliamos a expressão de 23nucleotídeo 3fosfodiesterase (CNPase) no córtex e cerebelo e a distribuição da NADPH-diaforase (NADPH-d) no cerebelo de ratos submetidos a este modelo de HI. Ratas no 18 dia de gestação foram anestesiadas, os cornos uterinos expostos e as 4 artérias uterinas obstruídas por 45 minutos (Grupo HI). Animais controle tiveram os úteros expostos sem sofrer a obstrução (Grupo Sham). Após a cirurgia a gestação prosseguiu. Somente animais nascidos a termo foram utilizados. Um terceiro grupo de animais não foi operado (Grupo NM). Após anestesia e perfusão-fixação com paraformaldeído 4% aos 9, 23 e 90 dias pós-natais, cortes coronais do prosencéfalo e parassagitais do cerebelo foram obtidos em criótomo e submetidos à imunohistoquímica para CNPase. Adicionalmente, cortes parassagitais do cerebelo obtidos em criótomo foram submetidos à histoquímica para NADPH-d. Observamos uma diminuição da imunorreatividade à CNPase no cingulum dos animais HI comparados aos animais NM e Sham em todas as idades. Em P9, nos animais HI, há menor número de células CNPase+ no cingulum e córtex motor. Aos 23 dias, há um menor número de células e fibras CNPase+ no córtex motor e mais corpos celulares no cingulum dos animais HI. Aos 90 dias, os animais HI apresentaram menos fibras no córtex motor que os animais controle. No cerebelo, observamos corpos celulares e fibras CNPase+ em regiões mais distais na folha 1 nos animais NM e Sham que nos animais HI aos 9 dias. A imunorreatividade à CNPase estava alterada na substância branca e nas fibras na substância cinzenta nos animais HI tanto aos 23 quanto aos 90 dias. A substância branca nos animais HI apresentaram maior numero de células marcadas para NADPH-d que os animais controle aos 9 e 23 dias, sendo que em P23 a marcação se encontrava tanto no corpo celular quanto nos prolongamentos. As células de Purkinje na folha 1 apresentaram marcação para NADPH-d+, tanto no corpo celular quanto na árvore dendrítica, nos animais NM e Sham, enquanto nos animais HI somente a árvore dendrítica apresentava marcação. Animais do grupo HI aos 23 dias apresentaram células NADPH-d+ na camada molecular das folhas 1, 6 e 10, sendo que animais dos grupos controle não apresentaram células NADPH-d+ nesta região. Este padrão de marcação se manteve nos animais adultos (P90). Nossos resultados mostram alterações na oligodendroglia que podem ser causadas por um menor número de células progenitoras, problemas na migração aos destinos finais e/ou atraso na diferenciação. Mostramos também que a HI perinatal altera a distribuição das células NADPH-d+ durante o desenvolvimento do cerebelo, com algumas destas alterações mantidas na vida adulta, indicando um dano permanente nesta… Advisors/Committee Members: Yael de Abreu Villaça, Penha Cristina Barradas Daltro Santos, Daniela Uziel Rozental, Flávia Carvalho Alcântara Gomes.

Subjects/Keywords: Neurofisiologia; Sistema motor; Hipóxia-isquqemia; Oligodendroglia; Neurophysiology; Motor system; Hypoxia-ischemia; Oligodendroglia; MORFOLOGIA

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

APA (6^th Edition):

Machado, T. S. C. (2008). Efeitos de lesão por hipóxia-isquemia pré-natal sobre o desenvolvimento do sistema motor: córtex e cerebelo. (Masters Thesis). Universidade do Estado do Rio de Janeiro. Retrieved from http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=2067 ;

Chicago Manual of Style (16^th Edition):

Machado, Tiago Savignon Cardoso. “Efeitos de lesão por hipóxia-isquemia pré-natal sobre o desenvolvimento do sistema motor: córtex e cerebelo.” 2008. Masters Thesis, Universidade do Estado do Rio de Janeiro. Accessed January 20, 2021. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=2067 ;.

MLA Handbook (7^th Edition):

Machado, Tiago Savignon Cardoso. “Efeitos de lesão por hipóxia-isquemia pré-natal sobre o desenvolvimento do sistema motor: córtex e cerebelo.” 2008. Web. 20 Jan 2021.

Vancouver:

Machado TSC. Efeitos de lesão por hipóxia-isquemia pré-natal sobre o desenvolvimento do sistema motor: córtex e cerebelo. [Internet] [Masters thesis]. Universidade do Estado do Rio de Janeiro; 2008. [cited 2021 Jan 20]. Available from: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=2067 ;.

Council of Science Editors:

Machado TSC. Efeitos de lesão por hipóxia-isquemia pré-natal sobre o desenvolvimento do sistema motor: córtex e cerebelo. [Masters Thesis]. Universidade do Estado do Rio de Janeiro; 2008. Available from: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=2067 ;

Universidade do Estado do Rio de Janeiro

3. Alan Pereira da Costa. Distribuição da caspase-3 clivada no cerebelo de ratos durante o desenvolvimento em um modelo de hipóxia-isquemia sistêmica pré-natal.

Degree: Master, 2015, Universidade do Estado do Rio de Janeiro

URL: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=9158 ;

► A Hipóxia-isquemia (HI) perinatal é um problema de saúde pública, e ocorrem aproximadamente 1,5 casos de encefalopatias por HI por 1000 nascidos vivos. Dos que… (more)

▼ A Hipóxia-isquemia (HI) perinatal é um problema de saúde pública, e ocorrem aproximadamente 1,5 casos de encefalopatias por HI por 1000 nascidos vivos. Dos que sobrevivem 25-60% sofrem de deficiências permanentes do desenvolvimento neurológico, incluindo paralisia cerebral, convulsões, retardo mental, e dificuldade de aprender. Neurônios e oligodendrócitos, especialmente os progenitores, são os mais afetados pela HI. Existem vários modelos de HI, no entanto, poucos levam em consideração as intercorrências maternas, a importância da atividade placentária, e as trocas entre mãe-filho, que são clinicamente observadas em humanos. Robinson estabeleceu um modelo de HI sistêmica pré-natal transitório, onde o fluxo das artérias uterinas da rata grávida era obstruído por 45 minutos no décimo oitavo dia (E18) de gestação. Neste modelo foram observadas alterações que são similares às observadas em cérebros humanos que passaram por hipóxia perinatal, dentre as quais foram relatados aumento no nível de apoptose. Caspase-3 é descrita como uma enzima que atua na apoptose, e é amplamente utilizada como marcador para células apoptóticas. Vários autores vêm mostrando, entretanto, que a enzima caspase-3 pode estar ativada para fins não apoptóticos. No modelo de HI sistêmica pré-natal, foram observados astrogliose na substância branca, morte de oligodendrócitos, lesão em axônios tanto na substância branca como no córtex cerebral, e danos motores. Pouco se sabe da influencia do insulto HI no desenvolvimento do cerebelo, considerando que o cerebelo junto com o córtex motor, contribui para o controle motor. O objetivo desse trabalho foi avaliar a distribuição da caspase-3 clivada durante o desenvolvimento do cerebelo em um modelo de HI pré-natal. Os resultados deste trabalho demonstram que as células caspase-3 clivadas apresentaram duas morfologias distintas em ambos os grupos. Uma onde a caspase-3 foi observada apenas no núcleo, oscilando entre células com imunorreatividade fraca a intensa, e de células com a presença da caspase-3 no corpo celular, nos prolongamentos condensados e presença de fragmentos ao redor do soma, morfologia típica de célula em apoptose. A HI pré-natal, assim como nos hemisférios cerebrais, levou ao aumento de células caspase-3 clivadas com morfologia de progenitores de oligodendrócitos no cerebelo do grupo HI em P2, mas não em P9 e P23. Também foi demonstrado que a HI pré-natal não levou a uma ativação da apoptose em oligodendrócitos, neurônios e microglia (identificados por seus respectivos marcadores, CNPase, NeuN e ED1) apresentando marcação no núcleos de células GFAP+, na substância branca, camada granular e nas células da glia de Bergmann, em P9 e P23 no cerebelo. Podemos concluir que a HI pré-natal aumentou o número de células imunorreativas para a caspase-3 em um período crítico do desenvolvimento da oligodendroglia no cerebelo, e que a diminuição de progenitores de oligodendrócitos no cerebelo decorrente do insulto pré-natal visto em trabalhos anteriores, pode estar relacionada a morte celular por… Advisors/Committee Members: Yael de Abreu Villaça, Anderson Ribeiro Carvalho, Penha Cristina Barradas Daltro Santos, Elizabeth Giestal de Araujo.

Subjects/Keywords: Apoptose; Oligodendroglia; Glia de Bergmann e Cerebelo; Apoptosis; Oligodendroglia; Bergmann Glia; Cerebellum; NEUROPSICOFARMACOLOGIA; Apoptose - Teses; Oligodendroglia - Teses; Caspase 3; Hipóxia fetal; Hipóxia-isquemia encefálica

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

APA (6^th Edition):

Costa, A. P. d. (2015). Distribuição da caspase-3 clivada no cerebelo de ratos durante o desenvolvimento em um modelo de hipóxia-isquemia sistêmica pré-natal. (Masters Thesis). Universidade do Estado do Rio de Janeiro. Retrieved from http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=9158 ;

Chicago Manual of Style (16^th Edition):

Costa, Alan Pereira da. “Distribuição da caspase-3 clivada no cerebelo de ratos durante o desenvolvimento em um modelo de hipóxia-isquemia sistêmica pré-natal.” 2015. Masters Thesis, Universidade do Estado do Rio de Janeiro. Accessed January 20, 2021. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=9158 ;.

MLA Handbook (7^th Edition):

Costa, Alan Pereira da. “Distribuição da caspase-3 clivada no cerebelo de ratos durante o desenvolvimento em um modelo de hipóxia-isquemia sistêmica pré-natal.” 2015. Web. 20 Jan 2021.

Vancouver:

Costa APd. Distribuição da caspase-3 clivada no cerebelo de ratos durante o desenvolvimento em um modelo de hipóxia-isquemia sistêmica pré-natal. [Internet] [Masters thesis]. Universidade do Estado do Rio de Janeiro; 2015. [cited 2021 Jan 20]. Available from: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=9158 ;.

Council of Science Editors:

Costa APd. Distribuição da caspase-3 clivada no cerebelo de ratos durante o desenvolvimento em um modelo de hipóxia-isquemia sistêmica pré-natal. [Masters Thesis]. Universidade do Estado do Rio de Janeiro; 2015. Available from: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=9158 ;

4. Preston, Marnie Anne. Novel mechanisms underlying hyaluronan-mediated remyelination failure.

Degree: PhD, 2011, Oregon Health Sciences University

URL: doi:10.6083/M4HM56FW ; http://digitalcommons.ohsu.edu/etd/677

Subjects/Keywords: Oligodendroglia; Demyelination; Hyaluronan; Oligodendroglia; Demyelinating Diseases; Hyaluronic Acid; Hyaluronoglucosaminidase

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APA (6^th Edition):

Preston, M. A. (2011). Novel mechanisms underlying hyaluronan-mediated remyelination failure. (Doctoral Dissertation). Oregon Health Sciences University. Retrieved from doi:10.6083/M4HM56FW ; http://digitalcommons.ohsu.edu/etd/677

Chicago Manual of Style (16^th Edition):

Preston, Marnie Anne. “Novel mechanisms underlying hyaluronan-mediated remyelination failure.” 2011. Doctoral Dissertation, Oregon Health Sciences University. Accessed January 20, 2021. doi:10.6083/M4HM56FW ; http://digitalcommons.ohsu.edu/etd/677.

MLA Handbook (7^th Edition):

Preston, Marnie Anne. “Novel mechanisms underlying hyaluronan-mediated remyelination failure.” 2011. Web. 20 Jan 2021.

Vancouver:

Preston MA. Novel mechanisms underlying hyaluronan-mediated remyelination failure. [Internet] [Doctoral dissertation]. Oregon Health Sciences University; 2011. [cited 2021 Jan 20]. Available from: doi:10.6083/M4HM56FW ; http://digitalcommons.ohsu.edu/etd/677.

Council of Science Editors:

Preston MA. Novel mechanisms underlying hyaluronan-mediated remyelination failure. [Doctoral Dissertation]. Oregon Health Sciences University; 2011. Available from: doi:10.6083/M4HM56FW ; http://digitalcommons.ohsu.edu/etd/677

Radboud University Nijmegen

5. Jeuken, Judith Willem Marie. (Cyto)genetic analysis of (oligodendro)glial tumors.

Degree: 2002, Radboud University Nijmegen

URL: http://hdl.handle.net/2066/19151

► The goal of the studies described in this thesis was to identify genetic markers with prognostic or therapeutic implications for the less common glial tumors,… (more)

Subjects/Keywords: Oligodendroglia; Ependymoma; Genanalyse; neurologie

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

APA (6^th Edition):

Jeuken, J. W. M. (2002). (Cyto)genetic analysis of (oligodendro)glial tumors. (Doctoral Dissertation). Radboud University Nijmegen. Retrieved from http://hdl.handle.net/2066/19151

Chicago Manual of Style (16^th Edition):

Jeuken, Judith Willem Marie. “(Cyto)genetic analysis of (oligodendro)glial tumors.” 2002. Doctoral Dissertation, Radboud University Nijmegen. Accessed January 20, 2021. http://hdl.handle.net/2066/19151.

MLA Handbook (7^th Edition):

Jeuken, Judith Willem Marie. “(Cyto)genetic analysis of (oligodendro)glial tumors.” 2002. Web. 20 Jan 2021.

Vancouver:

Jeuken JWM. (Cyto)genetic analysis of (oligodendro)glial tumors. [Internet] [Doctoral dissertation]. Radboud University Nijmegen; 2002. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/2066/19151.

Council of Science Editors:

Jeuken JWM. (Cyto)genetic analysis of (oligodendro)glial tumors. [Doctoral Dissertation]. Radboud University Nijmegen; 2002. Available from: http://hdl.handle.net/2066/19151

The Ohio State University

6. Bradel, Edward J. Studies on cultured neonatal rat oligodendrocytes.

Degree: PhD, Graduate School, 1982, The Ohio State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=osu1487171978756757

Subjects/Keywords: Biology; Oligodendroglia; Rats – Physiology

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

APA (6^th Edition):

Bradel, E. J. (1982). Studies on cultured neonatal rat oligodendrocytes. (Doctoral Dissertation). The Ohio State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=osu1487171978756757

Chicago Manual of Style (16^th Edition):

Bradel, Edward J. “Studies on cultured neonatal rat oligodendrocytes.” 1982. Doctoral Dissertation, The Ohio State University. Accessed January 20, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487171978756757.

MLA Handbook (7^th Edition):

Bradel, Edward J. “Studies on cultured neonatal rat oligodendrocytes.” 1982. Web. 20 Jan 2021.

Vancouver:

Bradel EJ. Studies on cultured neonatal rat oligodendrocytes. [Internet] [Doctoral dissertation]. The Ohio State University; 1982. [cited 2021 Jan 20]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1487171978756757.

Council of Science Editors:

Bradel EJ. Studies on cultured neonatal rat oligodendrocytes. [Doctoral Dissertation]. The Ohio State University; 1982. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1487171978756757

University of Texas Southwestern Medical Center

7. Battiste, James Douglas. Mash1 Defines Lineage Restricted Neuronal and Oligodendrocytic Precursor Cells in Spinal Cord Development.

Degree: 2007, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/570

► Recent advances have defined distinct neural progenitor and early interneuron pools in the developing spinal cord and the molecular events that influence progenitor cell fate.… (more)

▼ Recent advances have defined distinct neural progenitor and early interneuron pools in the developing spinal cord and the molecular events that influence progenitor cell fate. However, these early neurons have not been traced to adult neuron types. The transcription factor Mash1 is transiently expressed in a subset of neural progenitors and possesses a pro-neural function. The transient nature of its expression limits the ability to trace Mash1+ progenitors. To study the developing neural tube from progenitor to adult neuron, transgenic mouse strains were generated that express GFP, Cre recombinase, and tamoxifen-inducible Cre recombinase. The M1-GIC mouse line, showed faithful Mash1 expression recapitulation and traces Mash1+ progenitors mainly to dI3 and dI5 interneurons. This supports data from the Mash1 null mutant where these populations are decreased or absent. Using M1-GIC;R26R-lacZ mice, I was able to trace Mash1 expressing cells to neurons and oligodendrocytes in the adult mouse, but tracing to astrocytes was never observed. These data refute the conventional understanding that Mash1 is purely pro-neuronal, and is consistent with recent findings of Mash1 descendents in the early postnatal subventricular zone. Using M1-CRE-ER™;R26RlacZ and M1-CRE-ER™;R26R-YFP, Mash1+ cells trace into adulthood in a temporally-dependant manner. Cells expressing Mash1 at E10.5 become neurons of the dorsal horn in lamina I-IV while cells expressing Mash1 at E15.5 become oligodendrocytes spread over both gray and white matter. As a control, Nestin- CreERT2;R26R-lacZ and Nestin-CreERT2;R26R-YFP mice were used to confirm that common progenitors of all neural cell types can be traced from E10.5 to P21. This data provides evidence that Mash1 defines lineage restricted precursors that exit the cell cycle rapidly, and Mash1 is necessary for efficient loss of common progenitor characteristics as seen in the Mash1 null mutant. This data refines our understanding of progenitor characteristics and Mash1 function in the developing spinal cord. Advisors/Committee Members: Johnson, Jane E..

Subjects/Keywords: Gene Expression Regulation, Developmental; Neurons; Oligodendroglia

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APA (6^th Edition):

Battiste, J. D. (2007). Mash1 Defines Lineage Restricted Neuronal and Oligodendrocytic Precursor Cells in Spinal Cord Development. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/570

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):

Battiste, James Douglas. “Mash1 Defines Lineage Restricted Neuronal and Oligodendrocytic Precursor Cells in Spinal Cord Development.” 2007. Thesis, University of Texas Southwestern Medical Center. Accessed January 20, 2021. http://hdl.handle.net/2152.5/570.

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

MLA Handbook (7^th Edition):

Battiste, James Douglas. “Mash1 Defines Lineage Restricted Neuronal and Oligodendrocytic Precursor Cells in Spinal Cord Development.” 2007. Web. 20 Jan 2021.

Vancouver:

Battiste JD. Mash1 Defines Lineage Restricted Neuronal and Oligodendrocytic Precursor Cells in Spinal Cord Development. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2007. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/2152.5/570.

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

Council of Science Editors:

Battiste JD. Mash1 Defines Lineage Restricted Neuronal and Oligodendrocytic Precursor Cells in Spinal Cord Development. [Thesis]. University of Texas Southwestern Medical Center; 2007. Available from: http://hdl.handle.net/2152.5/570

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

University of Texas Southwestern Medical Center

8. He, Danyang. Epigenetic Regulation of Oligodendrocyte Development and Regeneration in the Central Nervous System.

Degree: 2016, University of Texas Southwestern Medical Center

URL: http://hdl.handle.net/2152.5/6142

► Oligodendrocytes (OLs) produce myelin sheaths that electrically insulate axons and promote rapid propagation of action potentials in the CNS. The onset and timing of CNS… (more)

▼ Oligodendrocytes (OLs) produce myelin sheaths that electrically insulate axons and promote rapid propagation of action potentials in the CNS. The onset and timing of CNS myelination and remyelination requires precise coordination between epigenetic programming and transcriptional regulation. In this thesis, I present my findings on two epigenetic regulatory complexes Chd7/Sox10 and lncOL1/Suz12 in CNS myelination and remyelination. First, we show that chromatin remodeler Chd7 is required for proper onset of CNS myelination and remyelination. Genome-occupancy analyses, coupled with transcriptome profiling, reveal that Chd7 interacts with Sox10 and targets the enhancers of key myelinogenic genes, and identify novel Chd7 targets including bone formation regulators Osterix/Sp7 and Creb3l2, which are also critical for oligodendrocyte maturation. Thus, Chd7 coordinates with Sox10 to regulate the initiation of myelinogenesis and acts as a molecular nexus of regulatory networks that account for the development of a seemingly diverse array of lineages including oligodendrocytes and osteoblasts, pointing to the hitherto previously uncharacterized Chd7 functions in white matter pathogenesis in CHARGE syndrome. To understand the role of lncRNAs in CNS myelination, we establish dynamic expression profiles of lncRNAs at different stages of oligodendrocyte development and uncover a cohort of stage-specific oligodendrocyte-restricted lncRNAs including a conserved chromatinassociated lncOL1. Genetic inactivation of lncOL1 causes defects in CNS myelination and remyelination following injury. Functional analyses illustrate that lncOL1 interacts with Suz12, a component of PRC2, to promote oligodendrocyte maturation in part through Suz12-mediated repression of a differentiation inhibitory network that maintains the precursor state. Collectively, these studies show that epigenetic circuitry between lncRNAs and transcription factors with chromatin-modifying complexes play roles in balancing inhibitory and activating gene program, allowing the timely CNS myelination and myelin repair. Advisors/Committee Members: Kraus, W. Lee, Lu, Q. Richard, Johnson, Jane E., Olson, Eric N..

Subjects/Keywords: Gene Expression Regulation, Developmental; Myelin Sheath; Oligodendroglia; RNA, Long Noncoding; Transcription Factors

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

APA (6^th Edition):

He, D. (2016). Epigenetic Regulation of Oligodendrocyte Development and Regeneration in the Central Nervous System. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/6142

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):

He, Danyang. “Epigenetic Regulation of Oligodendrocyte Development and Regeneration in the Central Nervous System.” 2016. Thesis, University of Texas Southwestern Medical Center. Accessed January 20, 2021. http://hdl.handle.net/2152.5/6142.

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

MLA Handbook (7^th Edition):

He, Danyang. “Epigenetic Regulation of Oligodendrocyte Development and Regeneration in the Central Nervous System.” 2016. Web. 20 Jan 2021.

Vancouver:

He D. Epigenetic Regulation of Oligodendrocyte Development and Regeneration in the Central Nervous System. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2016. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/2152.5/6142.

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

Council of Science Editors:

He D. Epigenetic Regulation of Oligodendrocyte Development and Regeneration in the Central Nervous System. [Thesis]. University of Texas Southwestern Medical Center; 2016. Available from: http://hdl.handle.net/2152.5/6142

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

Rutgers University

9. Gokina, Pradeepa, 1981-. The role of MAPKs in CNS demyelination.

Degree: Biology, 2013, Rutgers University

URL: https://rucore.libraries.rutgers.edu/rutgers-lib/41478/

Subjects/Keywords: Mitogen-activated protein kinases; Demyelination; Oligodendroglia

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APA (6^th Edition):

Gokina, Pradeepa, 1. (2013). The role of MAPKs in CNS demyelination. (Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/41478/

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):

Gokina, Pradeepa, 1981-. “The role of MAPKs in CNS demyelination.” 2013. Thesis, Rutgers University. Accessed January 20, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/41478/.

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

MLA Handbook (7^th Edition):

Gokina, Pradeepa, 1981-. “The role of MAPKs in CNS demyelination.” 2013. Web. 20 Jan 2021.

Vancouver:

Gokina, Pradeepa 1. The role of MAPKs in CNS demyelination. [Internet] [Thesis]. Rutgers University; 2013. [cited 2021 Jan 20]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/41478/.

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

Council of Science Editors:

Gokina, Pradeepa 1. The role of MAPKs in CNS demyelination. [Thesis]. Rutgers University; 2013. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/41478/

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

Universidade do Estado do Rio de Janeiro

10. Luiz Otávio Ribeiro de Lemos Felgueiras. A modulação da via do AMPc/PKA altera a morfologia da oligodendroglia e a distribuição das proteínas CNPase e MAG in vitro.

Degree: Master, 2012, Universidade do Estado do Rio de Janeiro

URL: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=9149 ;

►

A diferenciação da oligodendroglia depende de alterações coordenadas no citoesqueleto e na sua relação com a membrana plasmática, um componente importante para a formação da… (more)

▼

A diferenciação da oligodendroglia depende de alterações coordenadas no citoesqueleto e na sua relação com a membrana plasmática, um componente importante para a formação da bainha de mielina. A 23 nucleotídeo cíclico 3 fosfodiesterase (CNPase) está relacionada com a organização do citoesqueleto, sendo uma proteína ancoradoura de microtúbulos na membrana plasmática. In vitro, a CNPase compõe, com a F-actina e os microtúbulos, as estruturas semelhantes a nervuras ou os componentes radiais. A glicoproteína associada a mielina (MAG), também é importante para a formação dos véus de membrana e está associada a CNPase e a tubulina. Além disso, as três proteínas podem ser reguladas pela via de sinalização do AMPc/PKA. Buscando avaliar os efeitos da via do AMPc/PKA na regulação da diferenciação oligodendroglial, culturas de hemisférios cerebrais com 5 dias foram tratadas por 30 min ou 24 h com o inibidor (SQ22356-SQ [1 M]) ou com o ativador (forscolina [10M]) da adenilato ciclase ou com o inibidor da PKA, H-89 [1 M]. A oligodendroglia foi identificada pelo anticorpo anti-CNPase e por sua morfologia. Com 30 min de tratamento com forscolina, as células das culturas tratadas apresentaram prolongamentos maiores e menos véus de membrana quando comparadas às culturas controle. O tratamento com SQ também causou um aumento no tamanho dos prolongamentos e o tratamento com H-89 causou a redução no tamanho dos prolongamentos e nos véus de membrana. Com 24 h, as células tratadas com forscolina apresentaram poucos prolongamentos, já as culturas tratadas com SQ apresentaram um aumento no tamanho do prolongamento e as tratadas com H-89 demonstraram redução no véu de membrana. Observamos também alterações na distribuição da CNPase, tubulina e MAG, a primeira apresentou uma concentração próxima ao núcleo depois dos dois tempos de tratamento com H-89, o mesmo ocorreu com a tubulina. A CNPase adquiriu ainda um padrão puntiforme depois de 24 h de tratamento com ambos os inibidores. A MAG apresentou um aumento na concentração próximo ao núcleo depois de 30 min de tratamento com forscolina e SQ. O tratamento com SQ também reduziu a distribuição da MAG nos véus de membrana. A mesma redução foi observada depois de 24 h de tratamento com H-89. Esses resultados reforçam a participação da via do AMPc/PKA no desenvolvimento da oligodendroglia, incluindo a formação dos prolongamentos, suas ramificações e ainda a formação dos véus de membrana, com prováveis consequências na formação e manutenção da bainha de mielina.

Oligodendroglial differentiation depends on coordinated changes in the cytoskeleton and on its relationship with the plasmatic membrane, a critical site regarding the formation of the myelin sheath. 23cyclic nucleotide 3 phosphodiesterase (CNPase) is related to cytoskeleton modulation, anchoring microtubules to the plasmatic membrane. In vitro, CNPase composes, together with F-actin and microtubules, the vein-like structures or radial components in myelin sheath. Myelin associated glycoprotein (MAG) is important to membrane vellum…

Advisors/Committee Members: Iolanda Margherita Fierro, Penha Cristina Barradas Daltro Santos, Elizabeth Giestal de Araujo, Luciana Nogaroli Cavalcante.

Subjects/Keywords: Myelin proteins; Development; Oligodendrocyte; Proteínas de mielina; Via do AMPc/PKA; Desenvolvimento; Oligodendrócitos; CITOLOGIA E BIOLOGIA CELULAR; Oligodendroglia - Teses; Proteínas da Mielina; AMPc/PKA pathway

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

APA (6^th Edition):

Felgueiras, L. O. R. d. L. (2012). A modulação da via do AMPc/PKA altera a morfologia da oligodendroglia e a distribuição das proteínas CNPase e MAG in vitro. (Masters Thesis). Universidade do Estado do Rio de Janeiro. Retrieved from http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=9149 ;

Chicago Manual of Style (16^th Edition):

Felgueiras, Luiz Otávio Ribeiro de Lemos. “A modulação da via do AMPc/PKA altera a morfologia da oligodendroglia e a distribuição das proteínas CNPase e MAG in vitro.” 2012. Masters Thesis, Universidade do Estado do Rio de Janeiro. Accessed January 20, 2021. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=9149 ;.

MLA Handbook (7^th Edition):

Felgueiras, Luiz Otávio Ribeiro de Lemos. “A modulação da via do AMPc/PKA altera a morfologia da oligodendroglia e a distribuição das proteínas CNPase e MAG in vitro.” 2012. Web. 20 Jan 2021.

Vancouver:

Felgueiras LORdL. A modulação da via do AMPc/PKA altera a morfologia da oligodendroglia e a distribuição das proteínas CNPase e MAG in vitro. [Internet] [Masters thesis]. Universidade do Estado do Rio de Janeiro; 2012. [cited 2021 Jan 20]. Available from: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=9149 ;.

Council of Science Editors:

Felgueiras LORdL. A modulação da via do AMPc/PKA altera a morfologia da oligodendroglia e a distribuição das proteínas CNPase e MAG in vitro. [Masters Thesis]. Universidade do Estado do Rio de Janeiro; 2012. Available from: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=9149 ;

University of Louisville

11. Titsworth, William Lee. A possible role for sPLA2 in oligodendrocyte death and spinal cord injury.

Degree: PhD, 2008, University of Louisville

URL: 10.18297/etd/1445 ; https://ir.library.louisville.edu/etd/1445

► Spinal cord injury (SCI) can be divided into two distinct stages, an initial mechanical impact and a later "secondary injury" resulting from a cascade of… (more)

Subjects/Keywords: Spinal cord injury; Tumor necrosis factor; Oligodendroglia; Phospholipase A2; Hydrogen peroxide

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

APA (6^th Edition):

Titsworth, W. L. (2008). A possible role for sPLA2 in oligodendrocyte death and spinal cord injury. (Doctoral Dissertation). University of Louisville. Retrieved from 10.18297/etd/1445 ; https://ir.library.louisville.edu/etd/1445

Chicago Manual of Style (16^th Edition):

Titsworth, William Lee. “A possible role for sPLA2 in oligodendrocyte death and spinal cord injury.” 2008. Doctoral Dissertation, University of Louisville. Accessed January 20, 2021. 10.18297/etd/1445 ; https://ir.library.louisville.edu/etd/1445.

MLA Handbook (7^th Edition):

Titsworth, William Lee. “A possible role for sPLA2 in oligodendrocyte death and spinal cord injury.” 2008. Web. 20 Jan 2021.

Vancouver:

Titsworth WL. A possible role for sPLA2 in oligodendrocyte death and spinal cord injury. [Internet] [Doctoral dissertation]. University of Louisville; 2008. [cited 2021 Jan 20]. Available from: 10.18297/etd/1445 ; https://ir.library.louisville.edu/etd/1445.

Council of Science Editors:

Titsworth WL. A possible role for sPLA2 in oligodendrocyte death and spinal cord injury. [Doctoral Dissertation]. University of Louisville; 2008. Available from: 10.18297/etd/1445 ; https://ir.library.louisville.edu/etd/1445

University of Central Florida

12. Davis, Hedvika. Glial Differentiation Of Human Umbilical Stem Cells In 2d And 3d Environments.

Degree: 2011, University of Central Florida

URL: https://stars.library.ucf.edu/etd/2028

► During differentiation stem cells are exposed to a range of microenvironmental chemical and physical cues. In this study, human multipotent progenitor cells (hMLPCs) were differentiated… (more)

Subjects/Keywords: Astrocytes; Cell differentiation; Multipotent stem cells; Myelination; Noradrenaline; Noradrenergic mechanisms; Oligodendroglia; Stem cells; Surface chemistry; Umbilical cord; Medical Sciences; Dissertations, Academic – Medicine, Medicine – Dissertations, Academic

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

APA (6^th Edition):

Davis, H. (2011). Glial Differentiation Of Human Umbilical Stem Cells In 2d And 3d Environments. (Doctoral Dissertation). University of Central Florida. Retrieved from https://stars.library.ucf.edu/etd/2028

Chicago Manual of Style (16^th Edition):

Davis, Hedvika. “Glial Differentiation Of Human Umbilical Stem Cells In 2d And 3d Environments.” 2011. Doctoral Dissertation, University of Central Florida. Accessed January 20, 2021. https://stars.library.ucf.edu/etd/2028.

MLA Handbook (7^th Edition):

Davis, Hedvika. “Glial Differentiation Of Human Umbilical Stem Cells In 2d And 3d Environments.” 2011. Web. 20 Jan 2021.

Vancouver:

Davis H. Glial Differentiation Of Human Umbilical Stem Cells In 2d And 3d Environments. [Internet] [Doctoral dissertation]. University of Central Florida; 2011. [cited 2021 Jan 20]. Available from: https://stars.library.ucf.edu/etd/2028.

Council of Science Editors:

Davis H. Glial Differentiation Of Human Umbilical Stem Cells In 2d And 3d Environments. [Doctoral Dissertation]. University of Central Florida; 2011. Available from: https://stars.library.ucf.edu/etd/2028

University of Florida

13. Masters, Brian Andrew, 1962-. Insulin-like growth factors in cell differentiation and development in the nervous system.

Degree: 1990, University of Florida

URL: https://ufdc.ufl.edu/AA00056906

Subjects/Keywords: Astrocytes; Brain; Cultured cells; Insulin; Neurons; Oligodendroglia; Progenitor cells; Rats; Receptors; Somatomedins; Department of Physiology thesis Ph.D ( mesh ); Insulin-Like Growth Factor I ( mesh ); Nervous System – growth &; development ( mesh ); Oligodendroglia ( mesh ); Receptors, Somatomedin ( mesh ); Research ( mesh )

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

APA (6^th Edition):

Masters, Brian Andrew, 1. (1990). Insulin-like growth factors in cell differentiation and development in the nervous system. (Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/AA00056906

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):

Masters, Brian Andrew, 1962-. “Insulin-like growth factors in cell differentiation and development in the nervous system.” 1990. Thesis, University of Florida. Accessed January 20, 2021. https://ufdc.ufl.edu/AA00056906.

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

MLA Handbook (7^th Edition):

Masters, Brian Andrew, 1962-. “Insulin-like growth factors in cell differentiation and development in the nervous system.” 1990. Web. 20 Jan 2021.

Vancouver:

Masters, Brian Andrew 1. Insulin-like growth factors in cell differentiation and development in the nervous system. [Internet] [Thesis]. University of Florida; 1990. [cited 2021 Jan 20]. Available from: https://ufdc.ufl.edu/AA00056906.

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

Council of Science Editors:

Masters, Brian Andrew 1. Insulin-like growth factors in cell differentiation and development in the nervous system. [Thesis]. University of Florida; 1990. Available from: https://ufdc.ufl.edu/AA00056906

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

14. Kassler, Susannah W. Low molecular weight hyaluronic acid increases CD44 expression by oligodendrocytes and enhances inflammation.

Degree: MS, 2006, Oregon Health Sciences University

URL: doi:10.6083/M4QV3JS1 ; http://digitalcommons.ohsu.edu/etd/2889

Subjects/Keywords: Antigens, CD44; Hyaluronic Acid; Multiple Sclerosis – etiology; Oligodendroglia; T-Lymphocytes; Myelin Sheath; Encephalomyelitis, Autoimmune, Experimental

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APA (6^th Edition):

Kassler, S. W. (2006). Low molecular weight hyaluronic acid increases CD44 expression by oligodendrocytes and enhances inflammation. (Thesis). Oregon Health Sciences University. Retrieved from doi:10.6083/M4QV3JS1 ; http://digitalcommons.ohsu.edu/etd/2889

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):

Kassler, Susannah W. “Low molecular weight hyaluronic acid increases CD44 expression by oligodendrocytes and enhances inflammation.” 2006. Thesis, Oregon Health Sciences University. Accessed January 20, 2021. doi:10.6083/M4QV3JS1 ; http://digitalcommons.ohsu.edu/etd/2889.

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

MLA Handbook (7^th Edition):

Kassler, Susannah W. “Low molecular weight hyaluronic acid increases CD44 expression by oligodendrocytes and enhances inflammation.” 2006. Web. 20 Jan 2021.

Vancouver:

Kassler SW. Low molecular weight hyaluronic acid increases CD44 expression by oligodendrocytes and enhances inflammation. [Internet] [Thesis]. Oregon Health Sciences University; 2006. [cited 2021 Jan 20]. Available from: doi:10.6083/M4QV3JS1 ; http://digitalcommons.ohsu.edu/etd/2889.

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

Council of Science Editors:

Kassler SW. Low molecular weight hyaluronic acid increases CD44 expression by oligodendrocytes and enhances inflammation. [Thesis]. Oregon Health Sciences University; 2006. Available from: doi:10.6083/M4QV3JS1 ; http://digitalcommons.ohsu.edu/etd/2889

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

15. Stout, Randy Franklin. Calcium dynamics of glial cells and genetic influences on behavior of the nematode Caenorhabditis elegans.

Degree: PhD, 2011, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,1066

►

A major challenge in neuroscience is understanding how the different neural cell types work together to process information and produce a behavioral output. Glial cells… (more)

▼

A major challenge in neuroscience is understanding how the different neural cell types work together to process information and produce a behavioral output. Glial cells of the human brain have long been thought to act as support for the fundamental cell to cell communication at the core of cognition: neuronal synaptic communication. Research over the past several decades measuring glial activity and experimentally controlling glial cells in rodent model systems has shown that the two macroglia sub-types of glial cells (astrocytes and oligodendrocytes) have active roles in establishment, maintenance, and modulation of synaptic communication in the mammalian brain. Much of this research has utilized cell-type specific promoters to identify and genetically manipulate mammalian glial cells to better understand their role in intercellular communication in the brain. My research is aimed at examining the glia of C. elegans: a model organism chosen for a reductionist approach to research on how gene products and gene regulation work in development and function of a simple nervous system. I chose to focus on a subset of glia in this nematode, the sheath glia of the cephalic sensilla, due to cellular characteristics unique to this invertebrate and their morphological similarity to mammalian astrocytes and oligodendrocytes. I hypothesized that as the most evolutionarily ancient proto-astrocytes with some oligodendrocytes characteristics, these glia of C. elegans would exhibit a hallmark of mammalian glia: robust calcium dynamics upon stimulation. To test this hypothesis, I determined experimental applications for the hlh-17 gene promoter that would avoid confounding effects on behavior and used it to examine cultured C. elegans glia for the first time. I then adapted a genetically encoded calcium sensor to show that cultured glial cephalic sheath cells respond to membrane depolarization with increases in cytoplasmic calcium. I show that voltage-gated calcium channels underlie this response, indicating that glia of C. elegans have taken on a functional profile less like that known for mature mammalian glial cells but with some remaining commonalities. This establishes C. elegans as a model organism that can be used to study glia in a simple nervous system through contrast and comparison with macroglia of mammalian model organisms with similarities possibly representing ancient roles of glia and differences possibly representing roles taken on to meet demands imposed by a more complex nervous system.

1 online resource (xvi, 162 p.) : ill., digital, PDF file.

Neurobiology;

Joint Health Sciences;

glia Caenorhabditis elegans model organism astrocyte oligodendrocyte

UNRESTRICTED

Advisors/Committee Members: Parpura, Vladimir, Miller, Michael<br>, Pozzo-Miller, Lucas<br>, Sontheimer, Harald<br>, Yoder, Bradley.

Subjects/Keywords: Astrocytes – metabolism<; br>; Caenorhabditis elegans<; br>; Caenorhabditis elegans Proteins – metabolism<; br>; Calcium Channels, L-Type – metabolism<; br>; Neuroglia – metabolism<; br>; Oligodendroglia – metabolism

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APA (6^th Edition):

Stout, R. F. (2011). Calcium dynamics of glial cells and genetic influences on behavior of the nematode Caenorhabditis elegans. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,1066

Chicago Manual of Style (16^th Edition):

Stout, Randy Franklin. “Calcium dynamics of glial cells and genetic influences on behavior of the nematode Caenorhabditis elegans.” 2011. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 20, 2021. http://contentdm.mhsl.uab.edu/u?/etd,1066.

MLA Handbook (7^th Edition):

Stout, Randy Franklin. “Calcium dynamics of glial cells and genetic influences on behavior of the nematode Caenorhabditis elegans.” 2011. Web. 20 Jan 2021.

Vancouver:

Stout RF. Calcium dynamics of glial cells and genetic influences on behavior of the nematode Caenorhabditis elegans. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2011. [cited 2021 Jan 20]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1066.

Council of Science Editors:

Stout RF. Calcium dynamics of glial cells and genetic influences on behavior of the nematode Caenorhabditis elegans. [Doctoral Dissertation]. University of Alabama – Birmingham; 2011. Available from: http://contentdm.mhsl.uab.edu/u?/etd,1066

Vanderbilt University

16. Zannino, Denise Allison. Multiple roles for olig2 in the hindbrain: oligodendrocyte and abducens motor neuron specification and facial motor neuron migration.

Degree: PhD, Neuroscience, 2009, Vanderbilt University

URL: http://hdl.handle.net/1803/11277

► In the spinal cord, most oligodendrocytes, the myelinating cell type of the CNS, and motor neurons arise from common, ventral, olig2-expressing precursors called pMN cells.… (more)

Subjects/Keywords: Motor neurons – Growth; Oligodendroglia; neural precursors; hindbrain; olig2; oligodendrocyte; cranial motor neurons; zebrafish; Spinal cord – Growth

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

APA (6^th Edition):

Zannino, D. A. (2009). Multiple roles for olig2 in the hindbrain: oligodendrocyte and abducens motor neuron specification and facial motor neuron migration. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11277

Chicago Manual of Style (16^th Edition):

Zannino, Denise Allison. “Multiple roles for olig2 in the hindbrain: oligodendrocyte and abducens motor neuron specification and facial motor neuron migration.” 2009. Doctoral Dissertation, Vanderbilt University. Accessed January 20, 2021. http://hdl.handle.net/1803/11277.

MLA Handbook (7^th Edition):

Zannino, Denise Allison. “Multiple roles for olig2 in the hindbrain: oligodendrocyte and abducens motor neuron specification and facial motor neuron migration.” 2009. Web. 20 Jan 2021.

Vancouver:

Zannino DA. Multiple roles for olig2 in the hindbrain: oligodendrocyte and abducens motor neuron specification and facial motor neuron migration. [Internet] [Doctoral dissertation]. Vanderbilt University; 2009. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/1803/11277.

Council of Science Editors:

Zannino DA. Multiple roles for olig2 in the hindbrain: oligodendrocyte and abducens motor neuron specification and facial motor neuron migration. [Doctoral Dissertation]. Vanderbilt University; 2009. Available from: http://hdl.handle.net/1803/11277

17. Radošević Dragana. Морфолошка анализа нервних и глијалних ћелија главног маслинастог једра човека.

Degree: 2019, University of Novi Sad

URL: https://www.cris.uns.ac.rs/DownloadFileServlet/Disertacija156041008175697.pdf?controlNumber=(BISIS)110771&fileName=156041008175697.pdf&id=12985&source=OATD&language=en ; https://www.cris.uns.ac.rs/record.jsf?recordId=110771&source=OATD&language=en

► Главно маслинасто једро је највећи део доњег маслинастог комплекса. На пресеку главно маслинасто једро има изглед наборане врећице са дном које гледа ка спољашњој… (more)

▼ Главно маслинасто једро је највећи део доњег маслинастог комплекса. На пресеку главно маслинасто једро има изглед наборане врећице са дном које гледа ка спољашњој површини продужене мождине и отвором који је окренут унутра и дорзално. Главно маслинасто једро је укључено у просторну и временску организацију покрета и моторног учења, учења које је повезано са вежбањем, просуђивања времена интервала и брзине покретних стимулуса и когнитивних операција у простору. Популацију неурона главног маслинастог једра чине мултиполарни (90%) и интернеурони (10%). Дендритска арборизација неурона главног маслинастог једра је веома комплексна и различитог је облика (сферична или асиметрична), а правац пружања дендрита може да буде радијалан или кружан. Структурну и функционалну потпору неуронима пружају глијалне ћелије (астроцити, олигодендроцити и микроглија). Глијалне ћелије окружују неуроне и окупирају међунеуронске просторе где одржавају микросредину погодну за активност и виталност неурона. Старење представља природан и временски зависан процес који је карактерисан прогресивном појавом иреверзибилних промена у ћелијама, што резултира опадањем саморегулаторних способности јединке. У току старења, долази до нарушавања природног окружења неурона и глијалних ћелија што се одражава на њихов број, величину и изглед тела, дендритску крошњу и синаптичку организацију. Циљеви: Циљеви истраживања су да се утврди да ли се параметри морфологије неурона и глијалних ћелија разликују између старосних група, као и да се квантитативном анализом провери могућност класификације неурона и глијалних ћелија према квалитативном опису. Материјал и методе: Узорак студије је чинило 30 обостраних исечака главног маслинастог једра подељених у три старосне групе (други период сазревања (36-60 год.), рани период старења (61-75 год.) и касни период старења (76-90 год.)). Извршена је хистолошка обрада узорака Голџијевом методом импрегнације а микроскопске слике резова су дигитализоване а затим трансформисане у бинарне и скелетонизоване слике. Квалитативно су процењиване особине слика неурона (259) и глијалних ћелија (419) а квантитативна анализа величине, облика, гранања, дужине и сложености испитиваних ћелија спроведена је израчунавањем 22 (геометријска, компјутациона и фрактална) параметра. Резултати: Квалитативном проценом уочене су разлике у изгледу тела и неуронског поља, дендритске крошње, правца пружања дендрита, и распореда неурона у главном маслинастом једру. Квалитативна процена глијалних ћелија омогућила је њихов опис према врстама (астроцити, олигодендроцити и микроглија). Квантитативно испитивање геометријских параметара је показало да се неурони и глијалне ћелије не могу класификовати према величини. Неурони треће старосне групе имају мање вредности параметара који квантификују сложеност тела, неуронског поља и дендритске крошње, као и параметре дужине неурона. Површина тела, параметри дужине глијалне ћелије и сложеност глијалне крошње астроцита, значајно су мањи у узорку треће старосне групе, у поређењу са првом и другом. Олигодендроцити прве… Advisors/Committee Members: Marić Dušica, Milošević Nebojša, Stojšić-Džunja (Marković) Ljubica, Babović Siniša, Erić Mirela, Vlajković Slobodan, Krstonošić Bojana.

Subjects/Keywords: маслинасто једро; неурони; церебелум; глијалне ћелије; старење; старосни фактори; астроцити; олигодендроглијалне ћелије; морфолошки и микроскопски налази; maslinasto jedro; neuroni; cerebelum; glijalne ćelije; starenje; starosni faktori; astrociti; oligodendroglijalne ćelije; morfološki i mikroskopski nalazi; Оlivary nucleus; Neurons; Cerebellum; Neuroglia; Aging; Age factors; Astrocytes; Oligodendroglia; Morphological and Microscopic Findings

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

APA (6^th Edition):

Dragana, R. (2019). Морфолошка анализа нервних и глијалних ћелија главног маслинастог једра човека. (Thesis). University of Novi Sad. Retrieved from https://www.cris.uns.ac.rs/DownloadFileServlet/Disertacija156041008175697.pdf?controlNumber=(BISIS)110771&fileName=156041008175697.pdf&id=12985&source=OATD&language=en ; https://www.cris.uns.ac.rs/record.jsf?recordId=110771&source=OATD&language=en

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):

Dragana, Radošević. “Морфолошка анализа нервних и глијалних ћелија главног маслинастог једра човека.” 2019. Thesis, University of Novi Sad. Accessed January 20, 2021. https://www.cris.uns.ac.rs/DownloadFileServlet/Disertacija156041008175697.pdf?controlNumber=(BISIS)110771&fileName=156041008175697.pdf&id=12985&source=OATD&language=en ; https://www.cris.uns.ac.rs/record.jsf?recordId=110771&source=OATD&language=en.

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

MLA Handbook (7^th Edition):

Dragana, Radošević. “Морфолошка анализа нервних и глијалних ћелија главног маслинастог једра човека.” 2019. Web. 20 Jan 2021.

Vancouver:

Dragana R. Морфолошка анализа нервних и глијалних ћелија главног маслинастог једра човека. [Internet] [Thesis]. University of Novi Sad; 2019. [cited 2021 Jan 20]. Available from: https://www.cris.uns.ac.rs/DownloadFileServlet/Disertacija156041008175697.pdf?controlNumber=(BISIS)110771&fileName=156041008175697.pdf&id=12985&source=OATD&language=en ; https://www.cris.uns.ac.rs/record.jsf?recordId=110771&source=OATD&language=en.

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

Council of Science Editors:

Dragana R. Морфолошка анализа нервних и глијалних ћелија главног маслинастог једра човека. [Thesis]. University of Novi Sad; 2019. Available from: https://www.cris.uns.ac.rs/DownloadFileServlet/Disertacija156041008175697.pdf?controlNumber=(BISIS)110771&fileName=156041008175697.pdf&id=12985&source=OATD&language=en ; https://www.cris.uns.ac.rs/record.jsf?recordId=110771&source=OATD&language=en

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

Universidade do Estado do Rio de Janeiro

18. Viviane Younes Rapozo. Sinalização da MAPK/ERK na diferenciaçãao da oligodendroglia: efeitos de inibidores da MEK sobre a morfologia e distribuição de proteínas de oligodendrócitos/mielina in vitro.

Degree: PhD, 2009, Universidade do Estado do Rio de Janeiro

URL: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=9529 ;

►

A via de sinalização da cinase regulada por fatores extracelulares, da família das proteínas cinases ativadas por mitógenos (MAPK/ERK) é importante tanto para a sobrevivência… (more)

▼

A via de sinalização da cinase regulada por fatores extracelulares, da família das proteínas cinases ativadas por mitógenos (MAPK/ERK) é importante tanto para a sobrevivência como para a progressão da diferenciação de oligodendrócitos. Neste trabalho, a via da MAPK/ERK foi avaliada na oligodendroglia in vitro com a utilização de inibidores da MEK. A morfologia celular, assim como a distribuição de proteínas foram analisadas em diferentes estágios de maturação da oligodendroglia. Culturas primárias de oligodendrócitos foram tratadas com os inibidores da MEK PD98059 ou U0126, aos 5 ou 11dias in vitro (div), por 30min, 24 ou 48h. A oligodendroglia foi distinguida com marcadores estágio-específicos: A2B5, 23nucleotídeo cíclico 3 fosfodiesterase (CNPase) e proteína básica de mielina (MBP), e classificada de acordo com sua morfologia em diferentes estágios de desenvolvimento. O tratamento aumentou significativamente o número de células com morfologia mais imatura e diminuiu o número de células maduras. Além disso, aumentou o número de células redondas e sem prolongamentos as quais não puderam ser classificadas em nenhum dos estágios de desenvolvimento da oligodendroglia. Os efeitos mais evidentes foram observados logo após o menor tempo de tratamento. Células redondas eram positivas para CNPase e MBP, porém não foram marcadas com A2B5 ou com NG2, indicando que seriam células maduras incapazes de estender ou manter seus prolongamentos. De fato, estas mudanças foram acompanhadas por alterações na distribuição de proteínas de oligodendrócitos como a MBP e a CNPase, assim como alterações em proteínas de citoesqueleto, como actina, tubulina e na cinase de adesão focal (FAK). A MBP foi observada nas células tratadas em um padrão de distribuição desorganizado e disperso, oposto ao padrão contínuo que é observado nas células das culturas controle. Além disso, o tratamento causou uma desorganização na distribuição da CNPase, actina e tubulina. Nas células das culturas controle, estas proteínas apresentam um padrão organizado compondo as estruturas de citoqueleto semelhantes a nervuras. Após um pequeno período de tratamento (30min), actina e tubulina apresentaram o mesmo padrão de marcação puntiforme que a CNPase apresentou. O tratamento também reduziu os pontos de adesão focal demonstrados pela FAK. Com o decorrer do tratamento, após 24 e 48h, actina e tubulina aparentavam estar se reorganizando em um padrão filamentar. Estes resultados indicam um efeito importante da via da MAPK/ERK na ramificação e alongamento dos prolongamentos dos oligodendrócitos, com possíveis consequências para a formação da bainha de mielina.

The mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway is important for both long-term survival and timing of the progression of oligodendrocyte differentiation. In this work, the MAPK/ERK signaling in oligodendroglia was studied in vitro by using MEK inhibitors. Cell morphology and distribution of proteins were analyzed in different stages of maturation. Primary cultures of…

Advisors/Committee Members: Elizabeth Giestal de Araujo, Claudia dos Santos Mermelstein, Flávia Carvalho Alcântara Gomes, Frank Tenório de Almeida Costa, Penha Cristina Barradas Daltro Santos.

Subjects/Keywords: Oligodendrócito; Diferenciação; Via de sinalização MAPK/ERK; Citoesqueleto; Oligodendrocyte; Differentiation; MAPK/ERK signaling pathway; Cytoskeleton; CITOLOGIA E BIOLOGIA CELULAR; Oligodendroglia Teses; Bainha de mielina Doenças - Teses; Citoesqueleto - Teses; Sistema de sinalização das MAP Quinases

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

APA (6^th Edition):

Rapozo, V. Y. (2009). Sinalização da MAPK/ERK na diferenciaçãao da oligodendroglia: efeitos de inibidores da MEK sobre a morfologia e distribuição de proteínas de oligodendrócitos/mielina in vitro. (Doctoral Dissertation). Universidade do Estado do Rio de Janeiro. Retrieved from http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=9529 ;

Chicago Manual of Style (16^th Edition):

Rapozo, Viviane Younes. “Sinalização da MAPK/ERK na diferenciaçãao da oligodendroglia: efeitos de inibidores da MEK sobre a morfologia e distribuição de proteínas de oligodendrócitos/mielina in vitro.” 2009. Doctoral Dissertation, Universidade do Estado do Rio de Janeiro. Accessed January 20, 2021. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=9529 ;.

MLA Handbook (7^th Edition):

Rapozo, Viviane Younes. “Sinalização da MAPK/ERK na diferenciaçãao da oligodendroglia: efeitos de inibidores da MEK sobre a morfologia e distribuição de proteínas de oligodendrócitos/mielina in vitro.” 2009. Web. 20 Jan 2021.

Vancouver:

Rapozo VY. Sinalização da MAPK/ERK na diferenciaçãao da oligodendroglia: efeitos de inibidores da MEK sobre a morfologia e distribuição de proteínas de oligodendrócitos/mielina in vitro. [Internet] [Doctoral dissertation]. Universidade do Estado do Rio de Janeiro; 2009. [cited 2021 Jan 20]. Available from: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=9529 ;.

Council of Science Editors:

Rapozo VY. Sinalização da MAPK/ERK na diferenciaçãao da oligodendroglia: efeitos de inibidores da MEK sobre a morfologia e distribuição de proteínas de oligodendrócitos/mielina in vitro. [Doctoral Dissertation]. Universidade do Estado do Rio de Janeiro; 2009. Available from: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=9529 ;

Universidade do Estado do Rio de Janeiro

19. Tiago Savignon Cardoso Machado. Inibição do receptor de glutamato do tipo NMDA em um modelo de hipóxia-isquemia prenatal: avaliação morfofuncional do cerebelo.

Degree: PhD, 2013, Universidade do Estado do Rio de Janeiro

URL: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=5816 ;

► Lesões sistêmicas peri e pré-natais alteram o desenvolvimento do SNC, levando a problemas cognitivos e motores em crianças que podem perdurar por toda a vida.… (more)

▼ Lesões sistêmicas peri e pré-natais alteram o desenvolvimento do SNC, levando a problemas cognitivos e motores em crianças que podem perdurar por toda a vida. Um tipo particular de lesão é a hipóxia-isquemia (HI), caracterizada pela interrupção momentânea ou permanente do fluxo sanguíneo. Um dos mecanismos propostos para as lesões decorrentes da HI é a excitotoxicidade glutamatérgica. O uso de inibidores da neurotransmissão glutamatérgica tem sido estudados em diversos modelos de HI. Neste trabalho, avaliamos os efeitos morfofuncionais da administração de um antagonista não-competitivo do receptor de glutamato NMDA sobre o desenvolvimento do cerebelo. Ratas no 18 dia de gestação foram anestesiadas, os cornos uterinos expostos e as 4 artérias uterinas obstruídas por 45 minutos (Grupo H). Animais controle tiveram os úteros expostos, sem a obstrução (Grupo S). Após a cirurgia a gestação prosseguiu. Somente animais nascidos a termo foram utilizados. Um dia após o nascimento, metade de cada ninhada foi designada para receber MK801, 0,3mg/kg/dia, (grupos SM e HM) e a outra metade recebeu solução salina (grupos SS e HS), por 5 dias. Após anestesia e perfusão-fixação com paraformaldeído 4% aos 9, 23, 30 e 60 dias pós-natais, cortes parassagitais do cerebelo foram obtidos em criótomo e submetidos à imunohistoquímica para calbindina, GFAP, GLAST, PDGFRα e MBP. A partir de 45 dias de vida, os animais foram testados em vários de testes comportamentais: labirinto em cruz elevado (LCE), campo vazado (CV), ROTAROD, teste de caminhada sobre barras (ladder test) e teste do comprimento da passada (stride length). Aos 9 dias, a espessura da árvore dendrítica era menor nos animais SM, HS/HM, demonstrando efeitos deletérios tanto do MK801 quanto da HI. Menor número de células PDGFRα+ foi observado nos animais HS/HM, sem efeitos da administração de MK801. Aos 23 dias, maior número de células PDGFRα+ foi observado nos animais HM comparado aos outros 3 grupos, indicando efeito neuroprotetor do MK801. Nessa idade, menor número de fibras mielinizadas (MBP+) foi observada nos animais HS, e a administração de MK801 parece reverter estes efeitos. Aos 9 dias a distribuição de GLAST estava alterada nos animais HS, com os efeitos da HI parcialmente revertidos pelo MK801. Não foram observados efeitos da HI ou do MK801 sobre comportamentos relacionados a ansiedade pelo LCE, assim como na latência de queda no ROTAROD. HI piora a performance motora no ladder test. No teste do CV, não observamos efeitos da HI sobre a busca por novidade assim como sobre a atividade locomotora espontânea. No entanto, MK801 diminui comportamentos de autolimpeza e a atividade locomotora espontânea. Menor variação das passadas foi observada em decorrência da administração de MK801 no stride length, com nenhum efeito da HI. Nossos resultados demonstram que a inibição do receptor NMDA tem um efeito neuroprotetor sobre os progenitores de oligodendrócitos e mielinização, provavelmente pela manutenção da capacidade proliferativa por um período maior. A atividade… Advisors/Committee Members: Alex Christian Manhães, Cláudio Carneiro Filgueiras, Cecilia Hedin Pereira, Adriana da Cunha Faria Melibeu, Anderson Ribeiro Carvalho, Penha Cristina Barradas Daltro Santos.

Subjects/Keywords: Hipóxia-isquemia prenatal; Cerebelo; Receptor NMDA; Células de Purkinje; Oligodendrócitos; Mielina; Prenatal hipóxia-ischemia; Cerebellum; NMDA receptor; Purkinje cells; Oligodendrocytes; Myelin; NEUROFISIOLOGIA; Hipóxia Fetal; Cerebelo - Teses; Receptores de N-Metil-D-Aspartato; Células de Purkinje; Oligodendroglia Teses; Bainha de mielina - Teses

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

APA (6^th Edition):

Machado, T. S. C. (2013). Inibição do receptor de glutamato do tipo NMDA em um modelo de hipóxia-isquemia prenatal: avaliação morfofuncional do cerebelo. (Doctoral Dissertation). Universidade do Estado do Rio de Janeiro. Retrieved from http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=5816 ;

Chicago Manual of Style (16^th Edition):

Machado, Tiago Savignon Cardoso. “Inibição do receptor de glutamato do tipo NMDA em um modelo de hipóxia-isquemia prenatal: avaliação morfofuncional do cerebelo.” 2013. Doctoral Dissertation, Universidade do Estado do Rio de Janeiro. Accessed January 20, 2021. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=5816 ;.

MLA Handbook (7^th Edition):

Machado, Tiago Savignon Cardoso. “Inibição do receptor de glutamato do tipo NMDA em um modelo de hipóxia-isquemia prenatal: avaliação morfofuncional do cerebelo.” 2013. Web. 20 Jan 2021.

Vancouver:

Machado TSC. Inibição do receptor de glutamato do tipo NMDA em um modelo de hipóxia-isquemia prenatal: avaliação morfofuncional do cerebelo. [Internet] [Doctoral dissertation]. Universidade do Estado do Rio de Janeiro; 2013. [cited 2021 Jan 20]. Available from: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=5816 ;.

Council of Science Editors:

Machado TSC. Inibição do receptor de glutamato do tipo NMDA em um modelo de hipóxia-isquemia prenatal: avaliação morfofuncional do cerebelo. [Doctoral Dissertation]. Universidade do Estado do Rio de Janeiro; 2013. Available from: http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=5816 ;

University of Florida

20. Verrier, Jonathan. Post-Transcriptional Regulation of Myelin Genes by MicroRNAs.

Degree: PhD, Medical Sciences - Neuroscience (IDP), 2009, University of Florida

URL: https://ufdc.ufl.edu/UFE0041022

► The conduction of electrical signals along axons of the nerves is aided by the lipid-rich membrane, myelin, which is synthesized by glial cells. Myelination in… (more)

Subjects/Keywords: Axons; Genes; Messenger RNA; MicroRNAs; Myelin; Myelination; Oligodendroglia; Rats; RNA; Schwann cells; dicer, microrna, myelin, myelination, schwann

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

APA (6^th Edition):

Verrier, J. (2009). Post-Transcriptional Regulation of Myelin Genes by MicroRNAs. (Doctoral Dissertation). University of Florida. Retrieved from https://ufdc.ufl.edu/UFE0041022

Chicago Manual of Style (16^th Edition):

Verrier, Jonathan. “Post-Transcriptional Regulation of Myelin Genes by MicroRNAs.” 2009. Doctoral Dissertation, University of Florida. Accessed January 20, 2021. https://ufdc.ufl.edu/UFE0041022.

MLA Handbook (7^th Edition):

Verrier, Jonathan. “Post-Transcriptional Regulation of Myelin Genes by MicroRNAs.” 2009. Web. 20 Jan 2021.

Vancouver:

Verrier J. Post-Transcriptional Regulation of Myelin Genes by MicroRNAs. [Internet] [Doctoral dissertation]. University of Florida; 2009. [cited 2021 Jan 20]. Available from: https://ufdc.ufl.edu/UFE0041022.

Council of Science Editors:

Verrier J. Post-Transcriptional Regulation of Myelin Genes by MicroRNAs. [Doctoral Dissertation]. University of Florida; 2009. Available from: https://ufdc.ufl.edu/UFE0041022

21. Brill, Christina Victoria. The influence of oxygen on the development of oligodendroglia.

Degree: 2018, Freie Universität Berlin

URL: https://refubium.fu-berlin.de/handle/fub188/10703

► Oligondendroglia are cells of the central nervous system accounting for the myelinisation of signal transducing cells. Their development is a complex process not terminated at… (more)

▼ Oligondendroglia are cells of the central nervous system accounting for the myelinisation of signal transducing cells. Their development is a complex process not terminated at birth, especially not in prematurely born infants. Oligodendroglial precursor cells (OPCs) are highly susceptible to oxygen toxicity. As the in vivo oxygen saturation of the brain parenchyma is 3-7% we hypothesized that the 21% oxygen in room air commonly used in cell cultures may pose an oxygen challenge to OPCs. A classical cellular response to different oxygen concentrations is the adjustment of Hypoxia Inducible Factor 1 alpha (HIF-1α) activity. HIF-1α is known to influence several developmental processes such as proliferation and maturation. Oxygen can moreover cause oxidative stress. We cultured primary rat OPCs and cells of the oligodendroglia linage cell line OLN93 for 48 and 96 hours at 5 % and 21 % O2 and performed immunocytochemistry with antibodies against A2B5+ and O4+. Proliferation was quantified using Ki67 antibodies, TUNEL staining was applied to detect apoptosis. Gene expression of specific oligodendroglial transcription factors Olig1, Olig2, Sox9, Sox10, and also of maturation markers MBP and CNP were determined by realtime qPCR. Oxidative challenge in the cultures was assessed by gene expression Analysis of NRF2 and SOD2 and by Western blot analysis of nitrotyrosine. The role of HIF1a was investigated by HIF-1α luciferase reporter assay and comparison of results to cells with knockdown of HIF-1α. Morphology of OPCs differed between 21 % and 5 % O2 culture condition. After 48 hrs culture time, O4+ OL often showed multiple and complex processes at 5 % but had a much less differentiated structure at 21 % O2, as was revealed by Sholl analysis. Expression of MBP, CNP, Olig1, and Olig2 was significantly reduced, and antioxidant genes were significantly up- regulated after 48h at 21 % O2. Increased nitrotyrosine indicated oxidative stress at 21 % O2. There was no difference in apoptosis. At 21% O2, proliferation was reduced in OPCs and in OLN93 cells. Luciferease reporter Assay in transfected OLN93 cells indicated increased HIF-1α activity at 5 % O2. In OLN93 cells kept at 5 % O2, knockdown of HIF-1α caused a decrease in the expression of maturation markers MBP and CNP which was similar to that found at the higher oxygen level of 21 % O2. 21 % O2 impairs oligodendroglial development in vitro and oxidative stress and HIF-1α dysregulation seem to represent underlying mechanisms. Advisors/Committee Members: [email protected] (contact), w (gender), N.N. (firstReferee), N.N. (furtherReferee).

Subjects/Keywords: oligodendroglia; oxygen; brain development; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit

…have not yet been investigated with regards to the development of oligodendroglia. While the… …labeled using antibodies against A2B5 antigen and immature oligodendroglia were marked using… …immature O4+ oligodendroglia was observed after 48 and 96 hours (at 48 hours: 15.99 O4… …oligodendroglia. Culture conditions at 21% oxygen for 48 hours yielded significantly lower numbers of… …higher oxygen on proliferation of immature oligodendroglia (12.65% of O4+cells were also…

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APA (6^th Edition):

Brill, C. V. (2018). The influence of oxygen on the development of oligodendroglia. (Thesis). Freie Universität Berlin. Retrieved from https://refubium.fu-berlin.de/handle/fub188/10703

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):

Brill, Christina Victoria. “The influence of oxygen on the development of oligodendroglia.” 2018. Thesis, Freie Universität Berlin. Accessed January 20, 2021. https://refubium.fu-berlin.de/handle/fub188/10703.

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

MLA Handbook (7^th Edition):

Brill, Christina Victoria. “The influence of oxygen on the development of oligodendroglia.” 2018. Web. 20 Jan 2021.

Vancouver:

Brill CV. The influence of oxygen on the development of oligodendroglia. [Internet] [Thesis]. Freie Universität Berlin; 2018. [cited 2021 Jan 20]. Available from: https://refubium.fu-berlin.de/handle/fub188/10703.

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

Council of Science Editors:

Brill CV. The influence of oxygen on the development of oligodendroglia. [Thesis]. Freie Universität Berlin; 2018. Available from: https://refubium.fu-berlin.de/handle/fub188/10703

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

22. Friedrich, Vivien Leonie. Oligodendroglial maldevelopment in the cerebellum after postnatal hyperoxia and its prevention by minocycline.

Degree: 2017, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-7500

► Due to resend insides, brain injury after preterm birth often includes reduced cerebellar volume. During a phase of exponential growth, the neonatal cerebellum shows a… (more)

▼ Due to resend insides, brain injury after preterm birth often includes reduced cerebellar volume. During a phase of exponential growth, the neonatal cerebellum shows a high vulnerability to external stimuli. Underlying causes of cerebellar injury remain unclear. In general brain injury is caused by hypoxia-ischemia, infection and inflammation. In this study we analyzed whether postnatal hyperoxia perturbs white matter development in the cerebellum, and whether glial damage can be prevented by minocycline. For our experiments we used a well-established hyperoxia model. Six days old neonatal Wistar-rats (P6) were incubated with 80% oxygen for 24h until P7, followed by recovery in room air. Injections with minocycline were performed at the beginning and 12h during hyperoxia exposure. Hyperoxia induced oxidative stress in the cerebellum indicated by high nitrotyrosine levels. Higher numbers of TUNEL+ oligodendroglial precursor cells (OPC) showed increased apoptosis after high oxygen exposure. Hyperoxia affected OPC proliferation. The number of Ki67+NG2+ OPCs was reduced after exposure to hyperoxia at P7 and after recovering in room air until P11. Hyperoxia resulted in a decreased number of mature CC1+ oligodendroglia, indicating a perturbed maturation. Exposure to hyperoxia reduced the expression of MBP until P30. P30 and P60 MRI measurements and electron microscopy analyses of myelinated fibers at P30 exhibited a reduction of the cerebellar volume and a reduced thickness of the myelin sheath after exposure to hyperoxia from P6 to P7. Immunohistochemical stainings of Iba1 revealed no morphological activation of microglia after hyperoxia exposure. Increased expressions of PDGF-A in cerebellar tissue and cultured astrocytes indicated an impaired glia-glia-crosstalk caused by hyperoxia. The treatment with minocycline during hyperoxia exposure protected the immature cerebellum against white matter damage. We found attenuation of oxidative stress, reduced apoptosis, and improved oligodendroglial proliferation and maturation. MBP expression was improved, cerebellar volume reduction and hypomyelinisation was diminished by minocycline. Impaired glial crosstalk was improved by minocycline. The reduction of PDGF-A gene expression in the cerebellum and in primary astrocytes in cell culture was diminished by minocycline. In conclusion, oxidative stress caused by hyperoxia induces persistent white matter damage in the cerebellum. Treatment with minocycline attenuated the impairment and indicates possibilities of pharmacological prevention with anti-oxidative substances. Advisors/Committee Members: [email protected] (contact), w (gender), N.N. (firstReferee), N.N. (furtherReferee).

Subjects/Keywords: preterm infants; cerebellum; hyperoxia; white matter damage; minocycline; oligodendroglia; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit::610 Medizin und Gesundheit

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

APA (6^th Edition):

Friedrich, V. L. (2017). Oligodendroglial maldevelopment in the cerebellum after postnatal hyperoxia and its prevention by minocycline. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-7500

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):

Friedrich, Vivien Leonie. “Oligodendroglial maldevelopment in the cerebellum after postnatal hyperoxia and its prevention by minocycline.” 2017. Thesis, Freie Universität Berlin. Accessed January 20, 2021. http://dx.doi.org/10.17169/refubium-7500.

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

MLA Handbook (7^th Edition):

Friedrich, Vivien Leonie. “Oligodendroglial maldevelopment in the cerebellum after postnatal hyperoxia and its prevention by minocycline.” 2017. Web. 20 Jan 2021.

Vancouver:

Friedrich VL. Oligodendroglial maldevelopment in the cerebellum after postnatal hyperoxia and its prevention by minocycline. [Internet] [Thesis]. Freie Universität Berlin; 2017. [cited 2021 Jan 20]. Available from: http://dx.doi.org/10.17169/refubium-7500.

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

Council of Science Editors:

Friedrich VL. Oligodendroglial maldevelopment in the cerebellum after postnatal hyperoxia and its prevention by minocycline. [Thesis]. Freie Universität Berlin; 2017. Available from: http://dx.doi.org/10.17169/refubium-7500

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

Open Access Theses and Dissertations