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Am J Physiol Cell Physiol 274: C1290-C1297, 1998;
0363-6143/98 $5.00
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Vol. 274, Issue 5, C1290-C1297, May 1998

Neuropeptide Y inhibition of calcium channels in PC-12 pheochromocytoma cells

Laura A. McCullough, Terrance M. Egan, and Thomas C. Westfall

Department of Pharmacological and Physiological Science, Saint Louis University Health Sciences Center, St. Louis, Missouri 63104

We previously demonstrated, using rat PC-12 pheochromocytoma cells differentiated to a sympathetic neuronal phenotype with nerve growth factor (NGF), that neuropeptide Y (NPY) inhibits catecholamine synthesis as well as release. Inquiry into the mechanisms of these inhibitions implicated distinct pathways involving reduction of Ca2+ influx through voltage-activated Ca2+ channels. In the present investigation the effects of NPY on whole cell Ba2+ currents were examined to obtain direct evidence supporting the mechanisms suggested by those studies. NPY was found to inhibit the voltage-activated Ba2+ current in NGF-differentiated PC-12 cells in a reversible fashion with an EC50 of 13 nM. This inhibition was pertussis toxin sensitive and resulted from NPY modulation of L- and N-type Ca2+ channels. The inhibition of L-type channels was not seen with <1 nM free intracellular Ca2+ or when protein kinase C (PKC) was inhibited by chelerythrine or PKC-(19---31). Furthermore, the effect of NPY on L-type channels was mimicked by the PKC activator phorbol 12-myristate 13-acetate. These studies demonstrate that, in addition to inhibition of N-type Ca2+ channels, in NGF-differentiated PC-12 cells NPY inhibits L-type Ca2+ channels via an intracellular Ca2+- and PKC-dependent pathway.

nerve growth factor; omega -conotoxin GVIA; nifedipine; pertussis toxin


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