{"id":{"repo_id":"buffalo","oai_identifier":"oai:ubir.buffalo.edu:10477/80567"},"canonical_url":"https://search.dev.ndltd.org/etd/buffalo/oai:ubir.buffalo.edu:10477/80567","repository":{"repo_id":"buffalo","name":"Buffalo","base_url":"https://ubir.buffalo.edu/oai/request"},"display":{"title":"Regulation and Effect of Endothelial Acetylcholine on Oligodendrocyte Progenitor Cells","abstract":"M.S.","abstract_html":"M.S.","abstract_has_math":false,"creators":["Ravichandar, Roopa; 0000-0003-4888-2850"],"institution":"State University of New York at Buffalo","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Sim, Fraser","Neuroscience"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2019,"date_issued":"2019-10-28T15:32:56Z","date_published":"2019-10-28T15:32:56Z","updated_at":"2026-07-27T19:05:23Z","subjects":["neurosciences"],"languages":["eng"],"rights":["Users of works found in University at Buffalo Institutional Repository (UBIR) are responsible for identifying and contacting the copyright owner for permission to reuse. University at Buffalo Libraries do not manage rights for copyright-protected works and cannot assist with permissions.","Copyright retained by author."],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/10477/80567","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Sim, Fraser","Neuroscience"]},{"key":"dc:creator","label":"Author","values":["Ravichandar, Roopa; 0000-0003-4888-2850"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2019-10-28T15:32:56Z","2019","2019-07-19 11:27:34"]},{"key":"dc:publisher","label":"Institution","values":["State University of New York at Buffalo"]},{"key":"dc:type","label":"Dc Type","values":["Text","Thesis"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["neurosciences"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]},{"key":"dc:rights","label":"Dc Rights","values":["Users of works found in University at Buffalo Institutional Repository (UBIR) are responsible for identifying and contacting the copyright owner for permission to reuse. University at Buffalo Libraries do not manage rights for copyright-protected works and cannot assist with permissions.","Copyright retained by author."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/10477/80567"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["M.S.","Acetylcholine (ACh) plays an important role in inhibiting oligodendrocyte differentiation and remyelination through the activation of muscarinic receptors. However, the cellular source of acetylcholine involved in this signaling has not been established. Using a BAC transgenic ChAT GFP mouse model, we identified neuronal cells as a potential source of acetylcholine following lysolecithin demyelination. We obtained consistent results of neuronal ChAT expression in intraspinal inflammation caused by LPS which modelled inflammation inducing demyelination as observed in MS lesions. However, this does not exclude other non-neuronal sources of ACh released during remyelination. We hypothesized that ACh produced from endothelial cells acts on oligodendrocyte progenitor cells (OPCs) via M1/3 receptor and inhibits oligodendrocyte differentiation. To define the regulation of ChAT expression in intact brain, we performed flow cytometry analysis of ChAT-GFP mouse brain at postnatal day 7, day 14, and adult mice. We observed a very small fraction of endothelial cells expressing detectable ChAT GFP in the uninjured state. Intriguingly, following dissociation, isolated ChAT-GFP negative CD31+ endothelial cells progressively up-regulated GFP post sorting and seeding. This suggests that endothelial ACh expression may be induced by various environmental stimuli. Through co-culture experiments between hOPCs and human endothelial cells, we observed an increase in hOPC proliferation, however, we did not see an effect of endothelial cells on hOPC differentiation. Future experiments will investigate the mechanisms by which endothelial cells may act as potential modulators of hOPC proliferation and provide insight into the interplay between endothelial cells and OPCs in demyelinating diseases like MS."]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["Regulation and Effect of Endothelial Acetylcholine on Oligodendrocyte Progenitor Cells"]}]}],"canonical_facts":{"dc:contributor":["Sim, Fraser","Neuroscience"],"dc:creator":["Ravichandar, Roopa; 0000-0003-4888-2850"],"dc:date":["2019-10-28T15:32:56Z","2019","2019-07-19 11:27:34"],"dc:description":["M.S.","Acetylcholine (ACh) plays an important role in inhibiting oligodendrocyte differentiation and remyelination through the activation of muscarinic receptors. However, the cellular source of acetylcholine involved in this signaling has not been established. Using a BAC transgenic ChAT GFP mouse model, we identified neuronal cells as a potential source of acetylcholine following lysolecithin demyelination. We obtained consistent results of neuronal ChAT expression in intraspinal inflammation caused by LPS which modelled inflammation inducing demyelination as observed in MS lesions. However, this does not exclude other non-neuronal sources of ACh released during remyelination. We hypothesized that ACh produced from endothelial cells acts on oligodendrocyte progenitor cells (OPCs) via M1/3 receptor and inhibits oligodendrocyte differentiation. To define the regulation of ChAT expression in intact brain, we performed flow cytometry analysis of ChAT-GFP mouse brain at postnatal day 7, day 14, and adult mice. We observed a very small fraction of endothelial cells expressing detectable ChAT GFP in the uninjured state. Intriguingly, following dissociation, isolated ChAT-GFP negative CD31+ endothelial cells progressively up-regulated GFP post sorting and seeding. This suggests that endothelial ACh expression may be induced by various environmental stimuli. Through co-culture experiments between hOPCs and human endothelial cells, we observed an increase in hOPC proliferation, however, we did not see an effect of endothelial cells on hOPC differentiation. Future experiments will investigate the mechanisms by which endothelial cells may act as potential modulators of hOPC proliferation and provide insight into the interplay between endothelial cells and OPCs in demyelinating diseases like MS."],"dc:format":["application/pdf"],"dc:identifier":["http://hdl.handle.net/10477/80567"],"dc:language":["eng"],"dc:publisher":["State University of New York at Buffalo"],"dc:rights":["Users of works found in University at Buffalo Institutional Repository (UBIR) are responsible for identifying and contacting the copyright owner for permission to reuse. University at Buffalo Libraries do not manage rights for copyright-protected works and cannot assist with permissions.","Copyright retained by author."],"dc:subject":["neurosciences"],"dc:title":["Regulation and Effect of Endothelial Acetylcholine on Oligodendrocyte Progenitor Cells"],"dc:type":["Text","Thesis"]},"updated_at":"2026-07-27T19:05:23Z"}