P 343 Pathophysiological interpretation of retinal microcirculation based on a simulation model

EFFECT OF ISCHAEMIA ON SEROTONIN NEURONES IN THE RABBIT RETINA. CAZEVIEILLE C. and OSBORNE N.N. Nuftield Laboratory of Ophthalmology, University of Oxford, Oxford OX2 6AW, 1J.K. Serotonin is normally not present in sufficient concentrations in the rabbit retina for localisation by inununohistrxhemisby. The amine is taken up by a population of amacrine cells in the intact retina and in primary retinal cultures and can be viewed with immunohistochemistry. Accumulated scrotonin is released by kainate and AMPA in a dose dependent range and these processes are inhibited specifically by CNQX. Nh4DA, ACPD and APB did not cause a release of the accumulated serotonin. These data show that the semtonin neurones contain kainate/AMPA type receptors. Exposure of primary retinal cultures to kainate for a specific period or injectiml of kainate into the eye affected the serotonin cells in that they were eventually unable to accumulate exogenous serotonin. These data suggest that the kainate caused metabolic “death” to the semtonin cells. However, exposure of retinal cultures in glucose free medium and an absence of oxygen for 6 hours to induce ischaemia only affected some of the serotonin cells as a few of these neumnes still had the capacity to accumulate the amine. Similar data were determined for the intact retina where the intraocular pressure was raised above the systolic blood pressure for 90 mio but even after a repelfusion time of 6 days a few cells still accumulated serotonin. The combined data suggest that the rate of death of a serotonin cell due to ischaemia is dependent on the number of kainate/AhG’A receptors present. Acknowledgements: We are grateful for support from the EC.