BLOCKADE OF ISOPROTERENOL-INDUCED SYNAPTIC POTENTIATION BY TETRA-9-AMINOACRIDINE IN THE RAT AMYGDALA

The effects of tetrahydro-9-aminoacridine (THA) on P-adrenoceptor acti vation-induced synaptic potentiation were studied in brain slices of t he rat amygdala using intracellular recording techniques. To exclude t he involvement of N-methyl-D-aspartate (NMDA) receptors, all the exper iments were performed in the presence of NMDA receptor antagonist, D-A PV (50 mu M). Bath application of isoproterenol (Iso; 15 mu M) results in a long-lasting enhancement of the amplitude of excitatory postsyna ptic potentials (EPSPs) to 200+/-6% of baseline. Forskolin, which dire ctly activates adenyl cyclase, produces a similar effect suggesting th at Iso may act through a cyclic AMP-dependent mechanism. Pretreatment of the slices with THA (300 mu M) completely abolishes the Iso- and fo rskolin-induced synaptic potentiation. We hypothesize that the locus o f THA/beta-adrenoceptor interaction is presynaptic; the underlying mec hanism is likely due to THA's depression of transmitter release via a presynaptic blockade of voltage-dependent Ca2+ channels.