{"id":{"repo_id":"uwo","oai_identifier":"oai:uwo.scholaris.ca:20.500.14721/36037"},"canonical_url":"https://search.dev.ndltd.org/etd/uwo/oai:uwo.scholaris.ca:20.500.14721/36037","repository":{"repo_id":"uwo","name":"Western University","base_url":"https://uwo.scholaris.ca/server/oai/request"},"display":{"title":"Analyzing A-series gangliosides in neurons following exposure to glutamate","abstract":"Neurons within different brain regions have varying levels of vulnerability to external stress and therefore respond differently to injury. A potential reason to explain this may lie within a key lipid class of the cell’s plasma membrane called gangliosides. These glycosphingolipid species have been shown to play various roles in the maintenance of neuronal viability. The purpose of this study is to use electrospray ionization mass spectrometry (ESI-MS) technique and immunohistochemistry to evaluate the temporal changes in the expression profiles of various ganglioside species during the course of neurodegeneration in rat primary cortical neurons exposed to glutamate toxicity. Primary embryonic (E18) rat cortical neurons were cultured to DIV14. Glutamate toxicity was induced for 1, 3, 6 and 24 h. Immunofluorescence was used to stain for GM1 and GM3 species and ESI-MS was used to quantify the ganglioside species expressed within these injured neurons, which were compared to expression profiles of healthy neurons. Neurons were also pretreated with GM1 24 h before glutamate exposure to assess the level of neuroprotection conferred by GM1. Microglia were also activated using amyloid-beta oligomer and stained for GM1 and GM3 expression. ESI-MS data revealed that d16:1 and d18:1 GM1 species were upregulated in neurons exposed to glutamate while no significant changes were observed for GM2 and GM3 expression. Furthermore, neurons that were pretreated with GM1 showed increased viability compared to untreated neurons when exposed to glutamate. Immunofluorescence revealed an elevated expression of GM3 in activated microglia compared to controls. These data suggests that different gangliosides and cells within the CNS play diverse roles in the process of neurodegeneration.","abstract_html":"Neurons within different brain regions have varying levels of vulnerability to external stress and therefore respond differently to injury. A potential reason to explain this may lie within a key lipid class of the cell’s plasma membrane called gangliosides. These glycosphingolipid species have been shown to play various roles in the maintenance of neuronal viability. The purpose of this study is to use electrospray ionization mass spectrometry (ESI-MS) technique and immunohistochemistry to evaluate the temporal changes in the expression profiles of various ganglioside species during the course of neurodegeneration in rat primary cortical neurons exposed to glutamate toxicity. Primary embryonic (E18) rat cortical neurons were cultured to DIV14. Glutamate toxicity was induced for 1, 3, 6 and 24 h. Immunofluorescence was used to stain for GM1 and GM3 species and ESI-MS was used to quantify the ganglioside species expressed within these injured neurons, which were compared to expression profiles of healthy neurons. Neurons were also pretreated with GM1 24 h before glutamate exposure to assess the level of neuroprotection conferred by GM1. Microglia were also activated using amyloid-beta oligomer and stained for GM1 and GM3 expression. ESI-MS data revealed that d16:1 and d18:1 GM1 species were upregulated in neurons exposed to glutamate while no significant changes were observed for GM2 and GM3 expression. Furthermore, neurons that were pretreated with GM1 showed increased viability compared to untreated neurons when exposed to glutamate. Immunofluorescence revealed an elevated expression of GM3 in activated microglia compared to controls. These data suggests that different gangliosides and cells within the CNS play diverse roles in the process of neurodegeneration.","abstract_has_math":false,"creators":["Park, Dae Hee"],"institution":"The University of Western Ontario","degree_name":"M Sc","degree_level":null,"degree_discipline":"Anatomy and Cell Biology","degree_department":null,"school":null,"contributors":[],"advisors":["Whitehead, Shawn N.","Gilles A. 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In citing or referring to this thesis, use the DOI or handle from this page instead. Sample citation: Author name, \"Thesis title.\" (Year). Western University Open Repository. https://doi.org/10.71858/123456."]},{"key":"dc:description.abstract","label":"Abstract","values":["Neurons within different brain regions have varying levels of vulnerability to external stress and therefore respond differently to injury. A potential reason to explain this may lie within a key lipid class of the cell’s plasma membrane called gangliosides. These glycosphingolipid species have been shown to play various roles in the maintenance of neuronal viability. The purpose of this study is to use electrospray ionization mass spectrometry (ESI-MS) technique and immunohistochemistry to evaluate the temporal changes in the expression profiles of various ganglioside species during the course of neurodegeneration in rat primary cortical neurons exposed to glutamate toxicity. Primary embryonic (E18) rat cortical neurons were cultured to DIV14. Glutamate toxicity was induced for 1, 3, 6 and 24 h. Immunofluorescence was used to stain for GM1 and GM3 species and ESI-MS was used to quantify the ganglioside species expressed within these injured neurons, which were compared to expression profiles of healthy neurons. Neurons were also pretreated with GM1 24 h before glutamate exposure to assess the level of neuroprotection conferred by GM1. Microglia were also activated using amyloid-beta oligomer and stained for GM1 and GM3 expression. ESI-MS data revealed that d16:1 and d18:1 GM1 species were upregulated in neurons exposed to glutamate while no significant changes were observed for GM2 and GM3 expression. Furthermore, neurons that were pretreated with GM1 showed increased viability compared to untreated neurons when exposed to glutamate. Immunofluorescence revealed an elevated expression of GM3 in activated microglia compared to controls. These data suggests that different gangliosides and cells within the CNS play diverse roles in the process of neurodegeneration."]},{"key":"dc:title","label":"Title","values":["Analyzing A-series gangliosides in neurons following exposure to glutamate"]}]}],"canonical_facts":{"dc:contributor.advisor":["Whitehead, Shawn N.","Gilles A. Lajoie"],"dc:creator":["Park, Dae Hee"],"dc:date.accessioned":["2025-07-10T20:45:10Z"],"dc:date.available":["2025-07-10T20:45:10Z"],"dc:date.issued":["2015-08-13"],"dc:description":["The thesis cover page in the PDF document includes references to Western University’s previous institutional repository platform, known as Scholarship@Western, and links to that platform (beginning with ir.lib.uwo.ca). In citing or referring to this thesis, use the DOI or handle from this page instead. Sample citation: Author name, \"Thesis title.\" (Year). Western University Open Repository. https://doi.org/10.71858/123456."],"dc:description.abstract":["Neurons within different brain regions have varying levels of vulnerability to external stress and therefore respond differently to injury. A potential reason to explain this may lie within a key lipid class of the cell’s plasma membrane called gangliosides. These glycosphingolipid species have been shown to play various roles in the maintenance of neuronal viability. The purpose of this study is to use electrospray ionization mass spectrometry (ESI-MS) technique and immunohistochemistry to evaluate the temporal changes in the expression profiles of various ganglioside species during the course of neurodegeneration in rat primary cortical neurons exposed to glutamate toxicity. Primary embryonic (E18) rat cortical neurons were cultured to DIV14. Glutamate toxicity was induced for 1, 3, 6 and 24 h. Immunofluorescence was used to stain for GM1 and GM3 species and ESI-MS was used to quantify the ganglioside species expressed within these injured neurons, which were compared to expression profiles of healthy neurons. Neurons were also pretreated with GM1 24 h before glutamate exposure to assess the level of neuroprotection conferred by GM1. Microglia were also activated using amyloid-beta oligomer and stained for GM1 and GM3 expression. ESI-MS data revealed that d16:1 and d18:1 GM1 species were upregulated in neurons exposed to glutamate while no significant changes were observed for GM2 and GM3 expression. Furthermore, neurons that were pretreated with GM1 showed increased viability compared to untreated neurons when exposed to glutamate. Immunofluorescence revealed an elevated expression of GM3 in activated microglia compared to controls. These data suggests that different gangliosides and cells within the CNS play diverse roles in the process of neurodegeneration."],"dc:identifier.uri":["https://hdl.handle.net/20.500.14721/36037"],"dc:language.iso":["en_ca"],"dc:publisher":["The University of Western Ontario"],"dc:subject":["Glutamate Toxicity","Neurons","Central Nervous System","Neurodegeneration","Gangliosides","GM1","GM2","GM3","Neuroinflammation","Electrospray Ionization Mass Spectrometry","Microglia"],"dc:title":["Analyzing A-series gangliosides in neurons following exposure to glutamate"],"dc:type":["thesis"],"thesis:degree_discipline":["Anatomy and Cell Biology"],"thesis:degree_name":["M Sc"]},"updated_at":"2026-07-27T21:56:03Z"}