MODULATION OF CA2+ CHANNELS BY PROTEIN-KINASE-C IN RAT CENTRAL AND PERIPHERAL NEURONS - DISRUPTION OF G-PROTEIN-MEDIATED INHIBITION
MODULATION OF CA2+ CHANNELS BY PROTEIN-KINASE-C IN RAT CENTRAL AND PERIPHERAL NEURONS - DISRUPTION OF G-PROTEIN-MEDIATED INHIBITION
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DOI：
10.1016/0896-6273(93)90186-u
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发表时间：
1993-08-01
期刊：
影响因子：
16.2
通讯作者：
SWARTZ, KJ
中科院分区：
文献类型：
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作者：
SWARTZ, KJ
蛋白激酶 C (PKC) 的激活可减少多种中枢和外周神经元中谷氨酸、GABA(B)、腺苷、毒蕈碱、α-肾上腺素能和 LHRH 受体对 Ca2+ 通道的 G 蛋白依赖性抑制。 PKC 刺激还减轻了内部 GTPgammaS 的抑制作用，并减少了在不存在递质受体激动剂的情况下用内部 GTP 观察到的强直性 G 蛋白介导的抑制。在大多数研究的神经元中，PKC 刺激增强了基础 Ca2+ 通道电流。 PKC 诱导的基础电流增强是电压依赖性的，并且增强的电流表现出改变的动力学。用 GDPbetaS 抑制 G 蛋白可减弱 PKC 诱导的基础 Ca2+ 通道电流的增强。这些结果表明 PKC 可能通过破坏 G 蛋白与 Ca2+ 通道的偶联来调节 G 蛋白的抑制作用。 PKC 诱导的 Ca2+ 通道电流增强至少部分是由于消除了强直性 G 蛋白介导的抑制作用。
Activation of protein kinase C (PKC) reduced G protein-dependent inhibition of Ca2+ channels by glutamate, GABA(B), adenosine, muscarinic, alpha-adrenergic, and LHRH receptors in a variety of central and peripheral neurons. PKC stimulation also relieved the inhibitory effect of internal GTPgammaS and reduced tonic G protein-mediated inhibition observed with internal GTP in the absence of transmitter receptor agonist. Basal Ca2+ channel currents were enhanced by PKC stimulation in most neurons studied. The PKC-induced enhancement of basal current was voltage dependent, and enhanced currents displayed altered kinetics. Inhibition of G proteins with GDPbetaS attenuated the PKC-induced enhancement of basal Ca2+ channel current. These results show that PKC regulates the inhibitory effects of G proteins, possibly by disrupting the coupling of G proteins to Ca2+ channels. The PKC-induced enhancement of Ca2+ channel current results, at least in part, from the removal of tonic G protein-mediated inhibition.