@article {Huang2276, author = {Chiung-Chun Huang and Su-Jane Wang and Po-Wu Gean}, title = {Selective Enhancement of P-Type Calcium Currents by Isoproterenol in the Rat Amygdala}, volume = {18}, number = {6}, pages = {2276--2282}, year = {1998}, doi = {10.1523/JNEUROSCI.18-06-02276.1998}, publisher = {Society for Neuroscience}, abstract = {We investigated activation of β-adrenergic receptor{\textendash}adenylyl cyclase{\textendash}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.}, issn = {0270-6474}, URL = {https://www.jneurosci.org/content/18/6/2276}, eprint = {https://www.jneurosci.org/content/18/6/2276.full.pdf}, journal = {Journal of Neuroscience} }