Opposite regulation by the beta-adrenoceptor-cyclic AMP system of synaptic plasticity in the medial and lateral amygdala in vitro.

The effects of beta-adrenoceptor activation on short-term potentiation in the medial and lateral amygdala were investigated using rat brain slice preparations in vitro. Application of tetanic stimulation (100 pulses at 100 Hz) induced only short-term potentiation under normal recording conditions. In the medial amygdala, when the same tetanic stimulation was applied in the presence of a beta-adrenoceptor agonist, isoproterenol, short-term potentiation was significantly enhanced and long-term potentiation was induced. Phenylephrine, an alpha-adrenoceptor agonist, did not affect short-term potentiation. The short-term potentiation-enhancing effect of isoproterenol was mimicked by forskolin, an adenylate cyclase activator, and was blocked by Rp-adenosine-3',5'-cyclic-monophosphothioate, an inhibitor of cyclic AMP-dependent protein kinase. On the other hand, in the lateral amygdala, isoproterenol suppressed short-term potentiation. The short-term potentiation-suppressing effect of isoproterenol was mimicked by forskolin, and was blocked by Rp-adenosine-3',5'-cyclic-monophosphothioate. These results suggest that the beta-adrenoceptor-cyclic AMP system plays a role in facilitating the induction of long-term potentiation in the medial amygdala, but suppresses synaptic plasticity in the lateral amygdala.