Abstract
Pressure-induced ocular ischaemia followed by 25–28 hr of reperfusion to the rabbit retina drastically reduces or eliminates the b-wave of the electroretinogram and results in all the GABA from the amacrine cells being released, as judged by immunohistochemistry. Some of these GABA cells have the capacity to take-up exogenous serotonin and these GABA/serotonin cells have kainate/AMPA receptors. Previous studies have shown that an ischaemic insult causes these receptors to be stimulated to produce a release of the cells' GABA. The majority of the GABA/serotonin cells are also incapable of taking-up exogenous serotonin after ischaemia, which suggests that they are irreversibly damaged. However, there was still a minority of the cells which accumulated serotonin, which shows that neurones containing kainate/AMPA receptors are not irreversibly damaged at the same rate by ischaemia. The “staining” patterns for GABA A-receptor and GABA immunoreactivities in the rabbit retina are very similar and following ischaemia the GABA A-receptor immunoreactivity was reduced in intensity and became patchy in nature. It is not known whether this result reflects a down-regulation of the GABA A-receptors caused by the released GABA or a destruction of cells containing the GABA A-receptors. The ischaemic conditions used caused patchy, irregular and inconsistent signs of histological damage to the retina, even in areas of similar eccentricity, suggesting this parameter should be used with caution when judging the severity of an ischaemic insult. α-Protein kinase C (αPKC) present in the on-bipolar cells which have glutamate metabotropic APB receptors is both reduced or down-regulated and translocated by ischaemia. This is also the case for δ5PKC which is absent from the on-bipolar cells. These data were established by a combination of immunohistochemistry and electrophoresis/blotting experiments. Enzyme analysis also showed that all PKC calcium-dependent and -independent isoenzymes, are translocated and reduced by ischaemia making it difficult to judge whether PKC inhibitors may be appropriate anti-ischaemic agents.
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