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首页> 外文期刊>American Journal of Physiology >Neuropeptide Y inhibition of calcium channels in PC-12 pheochromocytoma cells.
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Neuropeptide Y inhibition of calcium channels in PC-12 pheochromocytoma cells.

机译：神经肽Y抑制PC-12嗜铬细胞瘤细胞中的钙通道。

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摘要

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 Ca(2+)- and PKC-dependent pathway.
机译：我们先前证明，使用分化为具有神经生长因子（NGF）的交感神经元表型的大鼠PC-12嗜铬细胞瘤细胞，神经肽Y（NPY）抑制儿茶酚胺的合成以及释放。对这些抑制机制的探讨涉及不同的途径，包括通过电压激活的Ca2 +通道减少Ca2 +流入。在本研究中，检查了NPY对全细胞Ba2 +电流的影响，以获得支持这些研究提出的机制的直接证据。发现NPY以可逆的方式抑制NGF分化的PC-12细胞中的电压激活的Ba2 +电流，EC50为13 nM。这种抑制作用是百日咳毒素敏感的，并且是由L型和N型Ca2 +通道的NPY调节引起的。用小于1 nM的游离细胞内Ca2 +或当白屈菜红碱或PKC-（19-31）抑制蛋白激酶C（PKC）时，未观察到L型通道的抑制作用。此外，PKY激活物佛波醇12-肉豆蔻酸酯13-乙酸酯模仿了NPY对L型通道的作用。这些研究表明，除了抑制N型Ca2 +通道外，在NGF分化的PC-12细胞中，NPY还通过细胞内Ca（2+）和PKC依赖性途径抑制L型Ca2 +通道。

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