FUNCTIONAL MODULATION OF BRAIN SODIUM-CHANNELS BY PROTEIN-KINASE-C PHOSPHORYLATION
FUNCTIONAL MODULATION OF BRAIN SODIUM-CHANNELS BY PROTEIN-KINASE-C PHOSPHORYLATION
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DOI：
10.1126/science.1656525
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发表时间：
1991-10-04
期刊：
影响因子：
56.9
通讯作者：
SCHEUER, T
中科院分区：
文献类型：
--
作者：
NUMANN, R;CATTERALL, WA;SCHEUER, T
负责脑中动作电位产生的电压门控钠通道被纯化形式的蛋白激酶C（PKC）磷酸化。 PKC的激活使钠电流峰值降低达80%，并减缓其对大鼠脑神经元中钠通道和中国仓鼠卵巢细胞中异源表达的大鼠脑IIA型钠通道α亚基的失活。 这些作用对PKC是特异性的，因为它们可以被PKC的特异性肽抑制剂阻断，并且可以通过将PKC直接应用于切除的由内而外的膜贴片中的钠通道的细胞质表面来再现。 PKC对脑钠通道的调节可能在中枢神经系统的信号转导和突触传递中起重要作用。
Voltage-gated sodium channels, which are responsible for the generation of action potentials in the brain, are phosphorylated by protein kinase C (PKC) in purified form. Activation of PKC decreases peak sodium current up to 80 percent and slows its inactivation for sodium channels in rat brain neurons and for rat brain type IIA sodium channel alpha-subunits heterologously expressed in Chinese hamster ovary cells. These effects are specific for PKC because they can be blocked by specific peptide inhibitors of PKC and can be reproduced by direct application of PKC to the cytoplasmic surface of sodium channels in excised inside-out membrane patches. Modulation of brain sodium channels by PKC is likely to have important effects on signal transduction and synaptic transmission in the central nervous system.