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Article: The selective vulnerability of retinal ganglion cells in rat chronic ocular hypertension model at early phase

TitleThe selective vulnerability of retinal ganglion cells in rat chronic ocular hypertension model at early phase
Authors
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. 8, p. 1143-1151 How to Cite?
AbstractGlutamate neurotoxicity has been postulated to play a prominent role in glaucoma. In this study the possible roles of two subunits of glutamate receptors during the early phase of retinal ganglion cell (RGC) loss in a rat chronic ocular hypertension (COH) model were investigated. COH was induced by applying argon laser to the episcleral and limbal veins of the right eye of rats, the observation times were at 4, 14 and 28 days after the first laser. RGCs were retrogradely labeled by putting Fluoro-Gold (FG) on the surface of both side superior colliculus. Immunohistochemical staining using specific antibodies against N-methyl-d-aspartate receptor 1 (NR1) or glutamate receptor 2/3 (GluR2/3) was performed on the retinal sections of normal and COH eyes. Fluorescent images were captured using confocal laser scanning microscope and the number of NR1 and GluR2/3 labeled cells were counted and cell size was measured using Stereo Investigator. During the observation period, the numbers of NR1 and GluR2/3 positive RGCs in the RGC layer were reduced parallel to the loss of RGC. The dramatic loss of GluR2/3 immunoreactive neurons occurred starting immediately after the first laser to 4 days while the dramatic loss of NR1 immunoreactive neurons occurred from 14 to 28 days after the first laser. Size difference was detected in NR1 immunoreactive RGCs, large ones were more sensitive to the high ocular pressure. These results suggest that both NR1 and GluR2/3 are involved in the mediation of RGC death in the early stage of COH. © 2009 Springer Science+Business Media, LLC.
Persistent Identifierhttp://hdl.handle.net/10722/58234
ISSN
2015 Impact Factor: 2.328
2015 SCImago Journal Rankings: 1.005
ISI Accession Number ID
Funding AgencyGrant Number
The University of Hong Kong Foundation for Educational Development and Research Limited
National Natural Science Foundation of China30170303
30671100
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. This study was also supported by the National Natural Science Foundation of China ( No 30170303 and 30671100). We would like to thank Mrs. CH So for her comments in the writing and Ms. Wen for her technical assistance in the use of the confocal microscope.

References

 

DC FieldValueLanguage
dc.contributor.authorLuo, XGen_HK
dc.contributor.authorChiu, Ken_HK
dc.contributor.authorLau, FHSen_HK
dc.contributor.authorLee, VWHen_HK
dc.contributor.authorYung, KKLen_HK
dc.contributor.authorSo, KFen_HK
dc.date.accessioned2010-05-31T03:26:19Z-
dc.date.available2010-05-31T03:26:19Z-
dc.date.issued2009en_HK
dc.identifier.citationCellular And Molecular Neurobiology, 2009, v. 29 n. 8, p. 1143-1151en_HK
dc.identifier.issn0272-4340en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58234-
dc.description.abstractGlutamate neurotoxicity has been postulated to play a prominent role in glaucoma. In this study the possible roles of two subunits of glutamate receptors during the early phase of retinal ganglion cell (RGC) loss in a rat chronic ocular hypertension (COH) model were investigated. COH was induced by applying argon laser to the episcleral and limbal veins of the right eye of rats, the observation times were at 4, 14 and 28 days after the first laser. RGCs were retrogradely labeled by putting Fluoro-Gold (FG) on the surface of both side superior colliculus. Immunohistochemical staining using specific antibodies against N-methyl-d-aspartate receptor 1 (NR1) or glutamate receptor 2/3 (GluR2/3) was performed on the retinal sections of normal and COH eyes. Fluorescent images were captured using confocal laser scanning microscope and the number of NR1 and GluR2/3 labeled cells were counted and cell size was measured using Stereo Investigator. During the observation period, the numbers of NR1 and GluR2/3 positive RGCs in the RGC layer were reduced parallel to the loss of RGC. The dramatic loss of GluR2/3 immunoreactive neurons occurred starting immediately after the first laser to 4 days while the dramatic loss of NR1 immunoreactive neurons occurred from 14 to 28 days after the first laser. Size difference was detected in NR1 immunoreactive RGCs, large ones were more sensitive to the high ocular pressure. These results suggest that both NR1 and GluR2/3 are involved in the mediation of RGC death in the early stage of COH. © 2009 Springer Science+Business Media, LLC.en_HK
dc.languageengen_HK
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0272-4340en_HK
dc.relation.ispartofCellular and Molecular Neurobiologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCell Sizeen_HK
dc.subject.meshCell Survivalen_HK
dc.subject.meshChronic Diseaseen_HK
dc.subject.meshDisease Models, Animalen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGlaucoma - metabolism - pathologyen_HK
dc.subject.meshIntraocular Pressure - physiologyen_HK
dc.subject.meshLight Coagulationen_HK
dc.subject.meshMicroscopy, Confocalen_HK
dc.subject.meshOcular Hypertension - pathology - physiopathologyen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshReceptors, AMPA - metabolismen_HK
dc.subject.meshReceptors, N-Methyl-D-Aspartate - metabolismen_HK
dc.subject.meshRetinal Ganglion Cells - metabolism - pathologyen_HK
dc.titleThe selective vulnerability of retinal ganglion cells in rat chronic ocular hypertension model at early phaseen_HK
dc.typeArticleen_HK
dc.identifier.emailSo, KF:hrmaskf@hkucc.hku.hken_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s10571-009-9407-1en_HK
dc.identifier.pmid19396539-
dc.identifier.scopuseid_2-s2.0-77049115014en_HK
dc.identifier.hkuros164014en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77049115014&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume29en_HK
dc.identifier.issue8en_HK
dc.identifier.spage1143en_HK
dc.identifier.epage1151en_HK
dc.identifier.isiWOS:000272781000009-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLuo, XG=7402870363en_HK
dc.identifier.scopusauthoridChiu, K=15076970500en_HK
dc.identifier.scopusauthoridLau, FHS=35519622900en_HK
dc.identifier.scopusauthoridLee, VWH=7402507569en_HK
dc.identifier.scopusauthoridYung, KKL=13605496000en_HK
dc.identifier.scopusauthoridSo, KF=34668391300en_HK
dc.identifier.citeulike4442880-

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