ANTIGENS ASSOCIATED WITH SPECIFIC RETINAL CELLS ARE AFFECTED BY ISCHAEMIA CAUSED BY RAISED INTRAOCULAR PRESSURE: EFFECT OF GLUTAMATE ANTAGONISTS * * Part of the work reported in this original communication was presented at the symposium entitled Excitatory Amino Acid Signaling , which was held in Kyoto, Japan, 15–18 July 1995 (organised by Y. Yoneda and M. Toru). Dr Yoneda also acted as executive editor in the processing of this manuscript.

ANTIGENS ASSOCIATED WITH SPECIFIC RETINAL CELLS ARE AFFECTED BY ISCHAEMIA CAUSED BY RAISED... Raising the rat's intraocular pressure above the systolic blood pressure for 60 min followed by a reperfusion of 7–10 days caused an ischaemic insult to the retina. The b-wave of the electroretinogram was abolished and the retinal thickness was much reduced, the greatest influence being associated with the inner retinal layers. No obvious histological damage was apparent at the light microscopy level. Immunocytochemistry, however, revealed a clear change in the nature of certain antigens associated with specific cell-types. Thy-1 antigen located to ganglion cell membranes was much reduced, suggesting that the ganglion cells are affected by ischaemia. Calretinin-immunoreactivity associated with amacrine cells is drastically reduced by ischaemia. In contrast, Ret-P1, located to the outer segments of the photoreceptors is unaffected by ischaemia. Ischaemia also caused GFAP-immunoreactivity to be expressed in the Müller cells, which is normally only associated with astrocytes in the ganglion/nerve fibre layer. Injection of a mixture of CNQX and MK-801, kainate and NMDA receptor antagonists, respectively, into the eye just before ischaemia failed to reverse the changes induced by the insult. However, analysis 3 days after reperfusion revealed that when the ischaemic insult was reduced to 45, rather than 60 min, the changes in the calretinin-immunoreactivity were reversed. The results show that immunocytochemistry provides a powerful way of following biochemical changes associated with specific cell types caused by ischaemia. Copyright © 1996 Elsevier Science Ltd. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Neurochemistry International Elsevier

ANTIGENS ASSOCIATED WITH SPECIFIC RETINAL CELLS ARE AFFECTED BY ISCHAEMIA CAUSED BY RAISED INTRAOCULAR PRESSURE: EFFECT OF GLUTAMATE ANTAGONISTS * * Part of the work reported in this original communication was presented at the symposium entitled Excitatory Amino Acid Signaling , which was held in Kyoto, Japan, 15–18 July 1995 (organised by Y. Yoneda and M. Toru). Dr Yoneda also acted as executive editor in the processing of this manuscript.

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Publisher
Elsevier
Copyright
Copyright © 1996 Elsevier Science Ltd
ISSN
0197-0186
DOI
10.1016/0197-0186(96)00005-8
Publisher site
See Article on Publisher Site

Abstract

Raising the rat's intraocular pressure above the systolic blood pressure for 60 min followed by a reperfusion of 7–10 days caused an ischaemic insult to the retina. The b-wave of the electroretinogram was abolished and the retinal thickness was much reduced, the greatest influence being associated with the inner retinal layers. No obvious histological damage was apparent at the light microscopy level. Immunocytochemistry, however, revealed a clear change in the nature of certain antigens associated with specific cell-types. Thy-1 antigen located to ganglion cell membranes was much reduced, suggesting that the ganglion cells are affected by ischaemia. Calretinin-immunoreactivity associated with amacrine cells is drastically reduced by ischaemia. In contrast, Ret-P1, located to the outer segments of the photoreceptors is unaffected by ischaemia. Ischaemia also caused GFAP-immunoreactivity to be expressed in the Müller cells, which is normally only associated with astrocytes in the ganglion/nerve fibre layer. Injection of a mixture of CNQX and MK-801, kainate and NMDA receptor antagonists, respectively, into the eye just before ischaemia failed to reverse the changes induced by the insult. However, analysis 3 days after reperfusion revealed that when the ischaemic insult was reduced to 45, rather than 60 min, the changes in the calretinin-immunoreactivity were reversed. The results show that immunocytochemistry provides a powerful way of following biochemical changes associated with specific cell types caused by ischaemia. Copyright © 1996 Elsevier Science Ltd.

Journal

Neurochemistry InternationalElsevier

Published: Sep 1, 1996

References

  • The influence of experimental ischaemia on protein kinase C and the GABAergic system in the rabbit retina
    Osborne, N.N.; Wood, J.; Muller, A.

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