We investigated activation of β-adrenergic receptor-adenylyl cyclase- cAMP cascade on the whole-cell voltage-dependent Ca(2+) currents (I(Ca) in acutely isolated rat basolateral amygdala neurons. Application of β-receptor agonist isoproterenol (Iso) caused a long-term enhancement of I(Ca). The effect of Iso was blocked by concurrent application of β-receptor antagonist propranolol. However, delayed application of propranolol after the/ca enhancement did not affect Iso-induced potentiation, suggesting that the sustained effect was not caused by a slow washout of Iso. Nimodipine and ω- conotoxin-GVIA reduced the I(ca) by ~35 and ~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 pretreatment with ω-agatoxin-IVA. Forskolin, an adenylyl cyclase activator, mimicked the action of Iso in enhancing I(Ca), 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 Ca(2+) channel blockers. These results suggest that P- type Ca(2+) channels were selectively upregulated in the basolateral amygdala neurons, and enhancement of P-type currents could contribute to presynaptic form of LTP.
|Number of pages||7|
|Journal||Journal of Neuroscience|
|Publication status||Published - 1998 Mar 15|
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