SELECTIVE ENHANCEMENT OF P-TYPE CALCIUM CURRENTS BY ISOPROTERENOL IN THE RAT AMYGDALA

We investigated activation of beta-adrenergic receptor-adenylyl cyclas e-cAMP cascade on the whole-cell voltage-dependent Ca2+ currents (I-Ca ) in acutely isolated rat basolateral amygdala neurons. Application of beta-receptor agonist isoproterenol (Iso) caused a long-term enhancem ent of I-Ca. The effect of Iso was blocked by concurrent application o f beta-receptor antagonist propranolol. However, delayed application o f propranolol after the I-Ca enhancement did not affect Iso-induced po tentiation, suggesting that the sustained effect was not caused by a s low washout of Iso. Nimodipine and omega-conotoxin-GVIA reduced the I- Ca by similar to 35 and similar to 29%, respectively, without reducing enhancement of I-Ca by Iso significantly, The modulation appeared to involve P-type current, because the enhancement was abolished after pr etreatment with omega-agatoxin-IVA. Forskolin, an adenylyl cyclase act ivator, mimicked the action of Iso in enhancing I-Ca, and this effect was blocked by an inhibitor of cAMP cascade, indicating a cAMP-depende nt mechanism. Iso also induced a long-term potentiation (LTP) of synap tic transmission, which could be prevented by P-type Ca2+ channel bloc kers. 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.