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The Journal of Neuroscience, March 15, 1998, 18(6):2276-2282

Selective Enhancement of P-Type Calcium Currents by Isoproterenol in the Rat Amygdala

Chiung-Chun Huang, Su-Jane Wang, and Po-Wu Gean

Department of Pharmacology, College of Medicine, National Cheng-Kung University, Tainan City, Taiwan 70101

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 ~35 and ~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.

Key words: isoproterenol; calcium channel; synaptic transmission; long-term potentiation; amygdala; cAMP


Copyright © 1998 Society for Neuroscience  0270-6474/98/1862276-07$05.00/0


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