INTERACTIONS OF N-ETHYLMALEIMIDE AND ALUMINUM FLUORIDE WITH GABA(B) RECEPTOR FUNCTION IN RAT NEOCORTICAL SLICES

Interactions of N-ethylmaleimide and aluminium fluoride (AIF(4)(-)) wi th GABA(B) receptors have been examined using spontaneously dischargin g rat neocortical slices. The suppression of discharges by the GABA(B) receptor agonist baclofen (5-10 mu M) was irreversibly prevented by N -ethylmaleimide (10-50 mu M) and its analog N-phenylmaleimide (10-50 m u M), whilst superfusion of slices with NaF (10 mM) and AlCl3 (100 mu M) to form a fluoroaluminate (AIF(4)(-)) complex markedly potentiated the action of baclofen. The lipoxygenase inhibitors, nordihydroguaiare tic acid (10-50 mu M) and eicosatetraynoic acid (10-50 mu M) or the ph ospholipase A(2) inhibitor bromophenacylbromide (50-100 mu M) did not affect the response to baclofen. The depressant action of baclofen is evidently mediated through G-proteins, but is not dependent on arachid onic acid metabolites.