PT  - JOURNAL ARTICLE
AU  - Chiung-Chun Huang
AU  - Su-Jane Wang
AU  - Po-Wu Gean
TI  - Selective Enhancement of P-Type Calcium Currents by Isoproterenol in the Rat Amygdala
AID  - 10.1523/JNEUROSCI.18-06-02276.1998
DP  - 1998 Mar 15
TA  - The Journal of Neuroscience
PG  - 2276--2282
VI  - 18
IP  - 6
4099  - http://www.jneurosci.org/content/18/6/2276.short
4100  - http://www.jneurosci.org/content/18/6/2276.full
SO  - J. Neurosci.1998 Mar 15; 18
AB  - We investigated activation of β-adrenergic receptor–adenylyl cyclase–cAMP cascade on the whole-cell voltage-dependent Ca2+ currents (ICa) in acutely isolated rat basolateral amygdala neurons. Application of β-receptor agonist isoproterenol (Iso) caused a long-term enhancement ofICa. The effect of Iso was blocked by concurrent application of β-receptor antagonist propranolol. However, delayed application of propranolol after theICa 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 theICa 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 ω-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.