ANTIGENS ASSOCIATED WITH SPECIFIC RETINAL CELLS ARE AFFECTED BY ISCHEMIA CAUSED BY RAISED INTRAOCULAR-PRESSURE - EFFECT OF GLUTAMATE ANTAGONISTS

Citation
Nn. Osborne et Ak. Larsen, ANTIGENS ASSOCIATED WITH SPECIFIC RETINAL CELLS ARE AFFECTED BY ISCHEMIA CAUSED BY RAISED INTRAOCULAR-PRESSURE - EFFECT OF GLUTAMATE ANTAGONISTS, Neurochemistry international, 29(3), 1996, pp. 263-270
Citations number
29
Categorie Soggetti
Biology,Neurosciences
ISSN journal
01970186
Volume
29
Issue
3
Year of publication
1996
Pages
263 - 270
Database
ISI
SICI code
0197-0186(1996)29:3<263:AAWSRC>2.0.ZU;2-J
Abstract
Raising the rat's intraocular pressure above the systolic blood pressu re for 60 min followed by a reperfusion of 7-10 days caused an ischaem ic insult to the retina. The b-wave of the electroretinogram was aboli shed and the retinal thickness was much reduced, the greatest influenc e being associated with the inner retinal layers. No obvious histologi cal damage was apparent at the light microscopy level. Immunocytochemi stry, however, revealed a clear change in the nature of certain antige ns associated with specific cell-types. Thy-1 antigen located to gangl ion cell membranes was much reduced, suggesting that the ganglion cell s are affected by ischaemia. Calretinin-immunoreactivity associated wi th amacrine cells is drastically reduced by ischaemia. In contrast, Re t-P1, located to the outer segments of the photoreceptors is unaffecte d by ischaemia. Ischaemia also caused GFAP-immunoreactivity to be expr essed in the Muller cells, which is normally only associated with astr ocytes in the ganglion/nerve fibre layer. Injection of a mixture of CN QX and MK-801, kainate and NMDA receptor antagonists, respectively, in to the eye just before ischaemia failed to reverse the changes induced by the insult. However, analysis 3 days after reperfusion revealed th at when the ischaemic insult was reduced to 45, rather than 60 min, th e changes in the calretinin-immunoreactivity were reversed. The result s show that immunocytochemistry provides a powerful way of following b iochemical changes associated with specific cell types caused by ischa emia. Copyright (C) 1996 Elsevier Science Ltd.