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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 -adrenergic receptor-adenylyl
cyclase-cAMP cascade on the whole-cell voltage-dependent
Ca2+ currents
(ICa) in acutely isolated rat
basolateral amygdala neurons. Application of -receptor agonist
isoproterenol (Iso) caused a long-term enhancement of
ICa. The effect of Iso was blocked by concurrent application of -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 -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
-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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