Interactions of N-ethylmaleimide and aluminium fluoride with GABA B receptor function in rat neocortical slices

Abstract

Interactions of N-ethylmaleimide and aluminium fluoride (AlF − 4) with GABA B receptors have been examined using spontaneously discharging rat neocortical slices. The suppression of discharges by the GABA B receptor agonst baclofen (5–10 μM) was irreversibly prevented by N-ethylmaleimide (10–50 μM) and its analog N-phenylmaleimide (10–50 μM), whilst superfusion of slices with NaF (10 mM) and AlCl 3 (100 μM) to form a fluoroaluminate (AlF − 4) complex markedly potentiated the action of baclofen. The lipoxygenase inhibitors, nordihydroguaiaretic acid (10–50 μM) and eicosatetraynoic acid (10–50 μM) or the phospholipase A 2 inhibitor bromophenacylbromide (50–100 μM) did not affect the response to baclofen. The depressant action of baclofen is evidently mediated through G-proteins, but is not dependent on arachidonic acid metabolites.