Blockade of isoproterenol-induced synaptic potentiation by tetra-9-aminoacridine in the rat amygdala.

The effects of tetrahydro-9-aminoacridine (THA) on beta-adrenoceptor activation-induced synaptic potentiation were studied in brain slices of the rat amygdala using intracellular recording techniques. To exclude the involvement of N-methyl-D-aspartate (NMDA) receptors, all the experiments were performed in the presence of NMDA receptor antagonist, D-APV (50 microM). Bath application of isoproterenol (Iso; 15 microM) results in a long-lasting enhancement of the amplitude of excitatory postsynaptic potentials (EPSPs) to 200 +/- 6% of baseline. Forskolin, which directly activates adenyl cyclase, produces a similar effect suggesting that Iso may act through a cyclic AMP-dependent mechanism. Pretreatment of the slices with THA (300 microM) completely abolishes the Iso- and forskolin-induced synaptic potentiation. We hypothesize that the locus of THA/beta-adrenoceptor interaction is presynaptic; the underlying mechanism is likely due to THA's depression of transmitter release via a presynaptic blockade of voltage-dependent Ca2+ channels.