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向海兔神经元R15内注射蛋白激酶抑制剂可阻断5-羟色胺诱导的钾离子电导增加。

Intracellular injection of protein kinase inhibitor blocks the serotonin-induced increase in K+ conductance in Aplysia neuron R15.

作者信息

Adams W B, Levitan I B

出版信息

Proc Natl Acad Sci U S A. 1982 Jun;79(12):3877-80. doi: 10.1073/pnas.79.12.3877.

Abstract

Previous work has shown that serotonin induces an increase in membrane K+ conductance in Aplysia neuron R15 and that this response is mediated by cAMP. The present study examines the role of protein phosphorylation in the response to serotonin. A specific inhibitor of cAMP-dependent protein kinase was injected intracellularly into neuron R15. The injection blocked the serotonin-induced increase in K+ conductance completely for at least 4 hours. The blockage was selective because the cell's response to dopamine was not inhibited. Furthermore, the blockage was specifically produced by protein kinase inhibitor because injection of other proteins (alpha-bungarotoxin and bovine serum albumin) did not affect the serotonin response. The serotonin response recovered fully 5-13 hours after the injection, presumably as a result of intracellular proteolysis of the protein kinase inhibitor. The results indicate that protein phosphorylation is a necessary step in the process that leads to activation of K+ channels by serotonin in neuron R15.

摘要

先前的研究表明,血清素可使海兔神经元R15的膜钾离子电导率增加,且该反应由环磷酸腺苷(cAMP)介导。本研究探讨了蛋白磷酸化在对血清素反应中的作用。将一种环磷酸腺苷依赖性蛋白激酶的特异性抑制剂细胞内注射到神经元R15中。该注射至少4小时内完全阻断了血清素诱导的钾离子电导率增加。这种阻断具有选择性,因为细胞对多巴胺的反应未受抑制。此外,这种阻断是由蛋白激酶抑制剂特异性产生的,因为注射其他蛋白质(α-银环蛇毒素和牛血清白蛋白)并不影响血清素反应。注射后5 - 13小时,血清素反应完全恢复,推测是由于蛋白激酶抑制剂在细胞内被蛋白水解。结果表明,蛋白磷酸化是血清素在神经元R15中激活钾离子通道过程中的一个必要步骤。

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