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Conference Paper: Glial influences on neuron survival and regeneration in the CNS environment

TitleGlial influences on neuron survival and regeneration in the CNS environment
Authors
KeywordsNeuroprotection
Neurotrophic factors
cytokines
apoptosis
Issue Date2001
PublisherSociety for Neuroscience.
Citation
The 31st Annual Meeting of Society for Neuroscience (Neuroscience 2001), San Diego, CA., 10–15 November 2001. How to Cite?
AbstractInflammation plays important role in limiting neuronal survival and axonal regeneration. Meanwhile, microglia and astrocytes are key players in mediating inflammation in CNS. Controlling inflammation thus is a crucial step in promoting neural survival and axonal regeneration. In our recent experiments, we have established an in vitro model to study inflammatory response in the CNS after ischemic (glucose and oxygen deprived)/hypoxic (oxygen deprived) injury. Methods: E-16 cortical neurons from rats were seeded on ischemic/hypoxic-injured glial cells, isolated from 1-day old rat brains, and co-cultured for 7 days. Using MAP2 immunocytochemistry, neuronal survival and neurite outgrowth were assessed by cell counts and image analysis (Neurolucider). Results: Our data suggest that small amount of inflammation (0.5 hr of ischemic treatment on glial cells) promotes neuronal survival and neurite extension. However, in longer ischemic/hypoxic-treated groups (>2hrs), both neuronal survival and neurite extension were decreased. Neurotrophic factors (NTF) are believed to modulate microglia, and glial cells have been known to release NTFs. However, detail mechanism on the regulation of NTFs by glial cells has not been fully understood. Our hypothesis is that the release of cytokines from the glial cells as a response to inflammation will decrease NTFs release, which leads to a decrease of neuronal survival and neurite extension. This abstract is sponsored by The Hong Kong Society of Neuroscience. Supported by the Hong Kong Regional Grant Council and The University of Hong Kong.
DescriptionPresentation no. 865.1
Persistent Identifierhttp://hdl.handle.net/10722/95763

 

DC FieldValueLanguage
dc.contributor.authorChui, AKMen_HK
dc.contributor.authorYip, HKFen_HK
dc.contributor.authorSo, KFen_HK
dc.contributor.authorWu, Wen_HK
dc.date.accessioned2010-09-25T16:12:28Z-
dc.date.available2010-09-25T16:12:28Z-
dc.date.issued2001en_HK
dc.identifier.citationThe 31st Annual Meeting of Society for Neuroscience (Neuroscience 2001), San Diego, CA., 10–15 November 2001.-
dc.identifier.urihttp://hdl.handle.net/10722/95763-
dc.descriptionPresentation no. 865.1-
dc.description.abstractInflammation plays important role in limiting neuronal survival and axonal regeneration. Meanwhile, microglia and astrocytes are key players in mediating inflammation in CNS. Controlling inflammation thus is a crucial step in promoting neural survival and axonal regeneration. In our recent experiments, we have established an in vitro model to study inflammatory response in the CNS after ischemic (glucose and oxygen deprived)/hypoxic (oxygen deprived) injury. Methods: E-16 cortical neurons from rats were seeded on ischemic/hypoxic-injured glial cells, isolated from 1-day old rat brains, and co-cultured for 7 days. Using MAP2 immunocytochemistry, neuronal survival and neurite outgrowth were assessed by cell counts and image analysis (Neurolucider). Results: Our data suggest that small amount of inflammation (0.5 hr of ischemic treatment on glial cells) promotes neuronal survival and neurite extension. However, in longer ischemic/hypoxic-treated groups (>2hrs), both neuronal survival and neurite extension were decreased. Neurotrophic factors (NTF) are believed to modulate microglia, and glial cells have been known to release NTFs. However, detail mechanism on the regulation of NTFs by glial cells has not been fully understood. Our hypothesis is that the release of cytokines from the glial cells as a response to inflammation will decrease NTFs release, which leads to a decrease of neuronal survival and neurite extension. This abstract is sponsored by The Hong Kong Society of Neuroscience. Supported by the Hong Kong Regional Grant Council and The University of Hong Kong.-
dc.languageengen_HK
dc.publisherSociety for Neuroscience.-
dc.relation.ispartofNeuroscience 2001en_HK
dc.subjectNeuroprotection-
dc.subjectNeurotrophic factors-
dc.subjectcytokines-
dc.subjectapoptosis-
dc.titleGlial influences on neuron survival and regeneration in the CNS environmenten_HK
dc.typeConference_Paperen_HK
dc.identifier.emailYip, HKF: hkfyip@hku.hken_HK
dc.identifier.emailSo, KF: hrmaskf@hkucc.hku.hken_HK
dc.identifier.emailWu, W: wtwu@hkucc.hku.hken_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.identifier.authorityWu, W=rp00419en_HK
dc.identifier.hkuros109271en_HK

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