Ong, J.Kerr, D.2006-06-232006-06-231995European Journal of Pharmacology, 1995; 287(2):197-2000014-29991879-0712http://hdl.handle.net/2440/5986Interactions of N-ethylmaleimide and aluminium fluoride (AlF - 4) with GABAB receptors have been examined using spontaneously discharging rat neocortical slices. The suppression of discharges by the GABAB receptor agonist baclofen (5-10 mu M) was irreversibly prevented by N-ethylmaleimide (10-50 mu M) and its analog N-phenylmaleimide (10-50 mu M), whilst superfusion of slices with NaF (10 mM) and AlCl3 (100 mu M) to form a fluoroaluminate (AlF - 4) complex markedly potentiated the action of baclofen. The lipoxygenase inhibitors, nordihydroguaiaretic acid (10-50 mu M) and eicosatetraynoic acid (10-50 mu M) or the phospholipase A2 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 arachidonic acid metabolites.enCerebral CortexAnimalsRatsRats, Sprague-DawleyAluminum CompoundsBaclofenEthylmaleimideReceptors, GABA-BMembrane PotentialsDrug InteractionsMaleJournal article0030006082001995046310.1016/0014-2999(95)00659-12-s2.0-002882666670088Ong, J. [0000-0002-0958-460X]