The intracellular mechanisms underlying the facilitatory action of isoproterenol (Iso) on the NMDA receptor-mediated synaptic potential (EPSPnmda) was investigated in an in vitro slice preparation of rat amygdala. Intracellular recordings were made from basolateral amygdala neurons in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 μM) and picrotoxin (50 μM) which block non-NMDA and GABAa receptors, respectively. Superfusion of Iso (15 μM) produced a sustained increase in EPSPnmda. Rp-adenosine-3′,5′-cyclic monophosphothioate (Rp-cAMPS), a potent inhibitor of protein kinase A (PKA) alone decreased the amplitude of EPSPnmda below baseline values and prevented the subsequent potentiation by Iso. Forskolin, a direct activator of adenylate cyclase, mimics the effect of Iso, and Rp-cAMPS also reversed forskolin-induced enhancement of EPSPnmda. These results suggest that cAMP-dependent protein kinase mediates the enhancement of EPSPnmda by Iso in the amygdala.
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