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

机译:胞内注射蛋白激酶抑制剂可阻止5-羟色胺诱导海ly神经元R15中K +电导的增加。

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摘要

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.
机译:先前的工作表明,5-羟色胺诱导海Ap神经元R15中的膜K +电导增加,并且这种反应是由cAMP介导的。本研究检查了蛋白质磷酸化在5-羟色胺反应中的作用。将cAMP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。注射完全阻断了血清素诱导的K +电导增加至少4小时。阻断是选择性的,因为细胞对多巴胺的反应没有被抑制。此外,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(α-邦加罗毒素和牛血清白蛋白)不会影响血清素的反应。注射后5至13小时,血清素反应完全恢复,大概是由于蛋白激酶抑制剂的细胞内蛋白水解作用。结果表明,蛋白质磷酸化是导致神经元R15中血清素激活K +通道的过程中必不可少的步骤。

著录项

  • 作者

    Adams, W B; Levitan, I B;

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  • 年度 1982
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  • 正文语种 en
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