Ischemia-related alteration of GABAA-operated chloride channel properties in gerbil hippocampus and cerebral cortex.

The properties of GABA-gated chloride (Cl-) channels in ischemia-reperfusion injury were studied by determination of the binding and dissociation kinetics of a specific Cl- channel ligand, tert-butylbicyclophosphoro[35S]thionate (TBPS) and by determination of 36CTl- uptake in the presence of the GABAA receptor agonist, muscimol. Four days after ischemia a small but insignificant decrease of [35S]TBPS binding to synaptic plasma membranes (SPM) was observed in the hippocampus and cerebral cortex as compared to control. The effect of ischemia was larger and statistically significant after the first and second month of reperfusion, constituting 20% inhibition of [35S]TBPS binding to SPM of sham-operated gerbils.