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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >cAMP-dependent, long-lasting inhibition of a K+ current in mammalian neurons.
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cAMP-dependent, long-lasting inhibition of a K+ current in mammalian neurons.

机译：cAMP依赖性，对哺乳动物神经元中K +电流的持久抑制。

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摘要

We report the long-term modulation of K+ channels by cAMP in cultured murine colliculi neurons. A short (1-2 s) application of 8-Br-cAMP induced a long-lasting broadening of the action potential, a loss of after-hyperpolarization, and a reduction in spike accommodation. In agreement with these changes, 8-Br-cAMP produced a long-lasting (2 hr) inhibition of a K+ current. These effects were also observed after a short activation of the pituitary adenylyl cyclase-activating polypeptide, beta-adrenergic, and 5-hydroxytryptamine type 4 (5-HT4) receptors, all known to increase cAMP. A transient activation of the cAMP-dependent protein kinase and a long-lasting inhibition of phosphatases (up to 2 hr) were detected. The blockade of the K+ current resulting from a brief application of 8-Br-cAMP or 5-hydroxytryptamine was prolonged from 2 to 4 hr when protein-serine/threonine phosphatases 1 and 2A were inhibited with 10 nM okadaic acid. The critical steps following the cAMP-dependent protein kinase activation and resulting in a long-term blockade of phosphatases are discussed in this report.
机译：我们报告了由培养的小鼠结肠神经元中的cAMP对K +通道的长期调节。短时间（1-2 s）施加8-Br-cAMP会引起动作电位的持久扩展，超极化后的丧失和峰适应性的降低。与这些变化一致，8-Br-cAMP对K +电流产生了持久的抑制作用（2小时）。在短暂激活垂体腺苷酸环化酶激活多肽，β-肾上腺素和4型5-羟色胺（5-HT4）受体（均已知可增加cAMP）后，也观察到了这些作用。检测到cAMP依赖性蛋白激酶的瞬时激活和磷酸酶的持久抑制（长达2小时）。当用10 nM冈田酸抑制蛋白质丝氨酸/苏氨酸磷酸酶1和2A时，短暂应用8-Br-cAMP或5-羟基色胺导致的K +电流阻滞延长2到4小时。本报告讨论了cAMP依赖性蛋白激酶激活并导致磷酸酶的长期阻断后的关键步骤。

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