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Article: Synaptic degeneration of retinal ganglion cells in a rat ocular hypertension glaucoma model

TitleSynaptic degeneration of retinal ganglion cells in a rat ocular hypertension glaucoma model
Authors
KeywordsC-fos
Glaucoma
Ocular hypertension
Retinal ganglion cell
Synapse
Issue Date2009
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0272-4340
Citation
Cellular And Molecular Neurobiology, 2009, v. 29 n. 4, p. 575-581 How to Cite?
AbstractAims Glaucoma is a common neurodegenerative disease that affects retinal ganglion cells (RGCs) and their axons. Little is known of the synaptic degeneration involved in the pathophysiology of glaucoma. Here we used an experimental ocular hypertension model in rats to investigate this issue. Methods Elevated intraocular pressure (IOP) was induced by laser coagulation of the episcleral and limbal veins. RGCs were retrogradely labeled with Fluoro-Gold (FG). The c-fos protein was used as a neuronal connectivity marker. Expression of c-fos in the retinas was investigated by immunohistochemistry at 5 days and 2 weeks after the induction of ocular hypertension. Both surviving RGCs as revealed by retrograde FG-labeled and c-fos-labeled RGCs were counted. Results The c-fos protein was mainly expressed in the nuclei and nucleoli of cells in the ganglion cell layer and inner nuclear layer in the normal retina. We also confirmed that c-fos was also expressed in the nuclei and nucleoli of RGCs retrogradely labeled with FG. There was no significant RGC loss at 5 days but about 13% RGC loss at 2 weeks after the induction of ocular hypertension. The number of RGCs expressing c-fos was significantly lower in the experimental animals at both 5 days and 2 weeks than normal. Conclusion Our study suggests that there is synaptic disconnection for RGCs after ocular hypertension and it may precede the cell death in the early stage. It may provide insight into novel therapeutic strategies to slow the progress of glaucoma. © 2009 Springer Science+Business Media, LLC.
Persistent Identifierhttp://hdl.handle.net/10722/149718
ISSN
2023 Impact Factor: 3.6
2023 SCImago Journal Rankings: 1.118
ISI Accession Number ID
Funding AgencyGrant Number
Guangdong National Science Foundation, China8451008901000852
National Science Foundation of China30801272
Funding Information:

This study was supported by funding from the Jessie Ho Professorship in Neuroscience (The University of Hong Kong Foundation for Educational Development and Research Limited, and donation from Mr. George Ho), and donations from Madame Tung Shai Yun, and Madame Annie Tsao Wen Wei. Part of this research is supported by the Grants of Guangdong National Science Foundation, China (8451008901000852) and National Science Foundation of China (30801272).

References

 

DC FieldValueLanguage
dc.contributor.authorFu, QLen_US
dc.contributor.authorLi, Xen_US
dc.contributor.authorShi, Jen_US
dc.contributor.authorXu, Gen_US
dc.contributor.authorWen, Wen_US
dc.contributor.authorLee, DHSen_US
dc.contributor.authorSo, KFen_US
dc.date.accessioned2012-06-26T05:57:35Z-
dc.date.available2012-06-26T05:57:35Z-
dc.date.issued2009en_US
dc.identifier.citationCellular And Molecular Neurobiology, 2009, v. 29 n. 4, p. 575-581en_US
dc.identifier.issn0272-4340en_US
dc.identifier.urihttp://hdl.handle.net/10722/149718-
dc.description.abstractAims Glaucoma is a common neurodegenerative disease that affects retinal ganglion cells (RGCs) and their axons. Little is known of the synaptic degeneration involved in the pathophysiology of glaucoma. Here we used an experimental ocular hypertension model in rats to investigate this issue. Methods Elevated intraocular pressure (IOP) was induced by laser coagulation of the episcleral and limbal veins. RGCs were retrogradely labeled with Fluoro-Gold (FG). The c-fos protein was used as a neuronal connectivity marker. Expression of c-fos in the retinas was investigated by immunohistochemistry at 5 days and 2 weeks after the induction of ocular hypertension. Both surviving RGCs as revealed by retrograde FG-labeled and c-fos-labeled RGCs were counted. Results The c-fos protein was mainly expressed in the nuclei and nucleoli of cells in the ganglion cell layer and inner nuclear layer in the normal retina. We also confirmed that c-fos was also expressed in the nuclei and nucleoli of RGCs retrogradely labeled with FG. There was no significant RGC loss at 5 days but about 13% RGC loss at 2 weeks after the induction of ocular hypertension. The number of RGCs expressing c-fos was significantly lower in the experimental animals at both 5 days and 2 weeks than normal. Conclusion Our study suggests that there is synaptic disconnection for RGCs after ocular hypertension and it may precede the cell death in the early stage. It may provide insight into novel therapeutic strategies to slow the progress of glaucoma. © 2009 Springer Science+Business Media, LLC.en_US
dc.languageengen_US
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0272-4340en_US
dc.relation.ispartofCellular and Molecular Neurobiologyen_US
dc.subjectC-fos-
dc.subjectGlaucoma-
dc.subjectOcular hypertension-
dc.subjectRetinal ganglion cell-
dc.subjectSynapse-
dc.subject.meshAnimalsen_US
dc.subject.meshApoptosis - Physiologyen_US
dc.subject.meshCaspases - Metabolismen_US
dc.subject.meshEnzyme Activationen_US
dc.subject.meshFemaleen_US
dc.subject.meshGlaucoma - Metabolism - Pathologyen_US
dc.subject.meshIntraocular Pressureen_US
dc.subject.meshNerve Degeneration - Metabolism - Pathologyen_US
dc.subject.meshOcular Hypertension - Metabolism - Pathologyen_US
dc.subject.meshProto-Oncogene Proteins C-Fos - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshRetina - Cytology - Metabolism - Pathologyen_US
dc.subject.meshRetinal Ganglion Cells - Cytology - Metabolism - Pathologyen_US
dc.subject.meshSynapses - Metabolism - Pathologyen_US
dc.titleSynaptic degeneration of retinal ganglion cells in a rat ocular hypertension glaucoma modelen_US
dc.typeArticleen_US
dc.identifier.emailSo, KF:hrmaskf@hkucc.hku.hken_US
dc.identifier.authoritySo, KF=rp00329en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/s10571-009-9349-7en_US
dc.identifier.pmid19172389-
dc.identifier.scopuseid_2-s2.0-67449159225en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67449159225&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume29en_US
dc.identifier.issue4en_US
dc.identifier.spage575en_US
dc.identifier.epage581en_US
dc.identifier.isiWOS:000266921200016-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridFu, QL=23388762000en_US
dc.identifier.scopusauthoridLi, X=36064257300en_US
dc.identifier.scopusauthoridShi, J=26025986700en_US
dc.identifier.scopusauthoridXu, G=7404263906en_US
dc.identifier.scopusauthoridWen, W=7102171038en_US
dc.identifier.scopusauthoridLee, DHS=7406670050en_US
dc.identifier.scopusauthoridSo, KF=34668391300en_US
dc.identifier.citeulike3981154-
dc.identifier.issnl0272-4340-

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