AbstractThe purpose of this study was to evaluate the function of the GABAAreceptor following transient forebrain ischaemia. The GABA‐stimulated chloride (36Cl−) uptake into synaptoneurosomes was determined as an indicator of GABAAreceptor function. Synaptoneurosomes were isolated from control rats and rats in which the forebrain was made ischaemic by way of the two‐vessel occlusion model. Animals subjected to ischaemia were killed at the end of the ischaemic insult and at 30 min or 2 or 5 h of recirculation. The results showed a reduction of 75 in GABA‐mediated36Cl−uptake in synaptoneurosomes isolated from animals shortly (<0.5 h) after the ischaemic episode (P<0.01). After longer recirculation periods the GABA‐mediated36Cl−uptake reached preischaemic control levels. To investigate whether alterations in36Cl−uptake were related to the synaptoneurosomal metabolic status, the synaptoneurosomal ATP content was measured. The time course of the ATP recovery correlated with the recovery of the GABA‐mediated36Cl−uptake (r= 0.7,P<0.001). To investigate the importance of ATP in GABA‐mediated36Cl−uptake more directly, synaptoneurosomes isolated from control rats were exposed to chemically induced ATP depletion with rotenone, an inhibitor of oxidative phosphorylation. This resulted in similar reductions in both ATP level and GABA‐stimulated36Cl−uptake as observed afterin vivoischaemia. These findings indicate that GABAAreceptor function is transiently impaired in the early postischaemic period in a way which is closely related to alterations in cellular energy metabolism. The relevance of these findings to the development of ischae
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