Selective enhancement of P-type calcium currents by isoproterenol in the rat amygdala.

We investigated activation of beta-adrenergic receptor-adenylyl cyclase-cAMP cascade on the whole-cell voltage-dependent Ca2+ currents (ICa) in acutely isolated rat basolateral amygdala neurons. Application of beta-receptor agonist isoproterenol (Iso) caused a long-term enhancement of ICa. The effect of Iso was blocked by concurrent application of beta-receptor antagonist propranolol. However, delayed application of propranolol after the ICa enhancement did not affect Iso-induced potentiation, suggesting that the sustained effect was not caused by a slow washout of Iso. Nimodipine and omega-conotoxin-GVIA reduced the ICa by approximately 35 and approximately 29%, respectively, without reducing enhancement of ICa by Iso significantly. The modulation appeared to involve P-type current, because the enhancement was abolished after pretreatment with omega-agatoxin-IVA. Forskolin, an adenylyl cyclase activator, mimicked the action of Iso in enhancing ICa, and this effect was blocked by an inhibitor of cAMP cascade, indicating a cAMP-dependent mechanism. Iso also induced a long-term potentiation (LTP) of synaptic transmission, which could be prevented by P-type Ca2+ channel blockers. These results suggest that P-type Ca2+ channels were selectively upregulated in the basolateral amygdala neurons, and enhancement of P-type currents could contribute to presynaptic form of LTP.