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首页> 外文学位 >Modulation of calcium channels in frog sympathetic neurons by ganglionic transmitters, G proteins and intracellular messengers.
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Modulation of calcium channels in frog sympathetic neurons by ganglionic transmitters, G proteins and intracellular messengers.

机译：神经节递质，G蛋白和细胞内信使调节青蛙交感神经元中的钙通道。

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摘要

Frog sympathetic neurons have been widely used as a model system for studying regulation of neuronal excitability. These cells exhibit robust slow synaptic potentials resulting from modulation of ion channels active at resting or weakly depolarized membrane potentials. The M-current, a voltage-dependent K+ current, can be inhibited by actions of endogenous ganglionic transmitters such as acetylcholine (ACh), epinephrine (EPI), luteinizing hormone-releasing hormone (LHRH) or substance P (SP). Decreased K+ conductances, along with an increased leak conductance, play a major role in generating slow excitatory postsynaptic potentials (EPSPs). Any of the endogenous neurotransmitters could affect voltage-gated Ca2+ channels. Effects on Ca 2+ entry might be important in understanding sympathetic physiology.; The effects of LHRH, SP, ACh, and EPI on Ca2+ channels and M- and leak currents of frog sympathetic neurons were studied. LHRH, SP and EPI effectively inhibited N-type Ca2+ currents and M-type K+ currents. The notable exception was ACh, which had little effect on high-voltage activated Ca2+ channels, even when it almost completely blocked the M-current. LHRH also induced a leak conductance. The peptidergic inhibition of Ca2+ channels was mimicked by cytoplasmic GTPγS but not by modulators of protein kinases, consistent with the involvement of a G Protein, but not protein phosphorylation. No evidence for the involvement of intracellular messengers was found.; LHRH decreased Ca2+-activated K+ current, most likely as a consequence of the inhibition of Ca2+ influx. Inhibition of this K+ current would result in prolonged action potentials, reduced afterhyperpolarizations, and increased excitability, in synergy with the effects of M-current suppression. On the other hand, LHRH also decreased transmitter release evoked by K+ depolarization. Thus, modulation of Ca2+ channels plays a prominent role, along with M-current suppression and leak current induction, in the overall regulation of ganglionic function by neurotransmitters.
机译：青蛙交感神经元已被广泛用作研究神经元兴奋性调节的模型系统。这些细胞表现出强健的缓慢突触电位，其起因于对处于静止或弱去极化膜电位的离子通道的调节。 M电流是电压依赖性K + 电流，可通过内源性神经节性递质（如乙酰胆碱（ACh），肾上腺素（EPI），促黄体生成激素释放激素（LHRH）或物质P（SP）。 K + 电导的减少以及泄漏电导的增加在产生缓慢的兴奋性突触后突触电位（EPSPs）中起主要作用。任何内源性神经递质均可影响电压门控的Ca 2 + 通道。 Ca 2 + 的进入可能对理解交感生理很重要。研究了LHRH，SP，ACh和EPI对青蛙交感神经元Ca 2 + 通道及M-和漏电流的影响。 LHRH，SP和EPI有效抑制N型Ca 2 + 电流和M型K + 电流。值得注意的例外是ACh，即使它几乎完全阻断了M电流，它对高压激活的Ca 2 + 通道也几乎没有影响。 LHRH还引起泄漏电导。 Ca 2 + 通道对肽的抑制作用被细胞质的GTPγS所模仿，而不是被蛋白激酶的调节剂所模仿，这与G蛋白的参与而不是蛋白的磷酸化相一致。没有发现细胞内信使参与的证据。 LHRH降低了Ca 2 + 激活的K + 电流，最有可能是由于Ca 2 + 内流的抑制所致。与M电流抑制作用协同作用，抑制该K + 电流将导致动作电位延长，后超极化减少和兴奋性增加。另一方面，LHRH也降低了K + 去极化引起的发射器释放。因此，在神经递质对神经节功能的整体调节中，Ca 2 + 通道的调制以及M电流抑制和泄漏电流诱导起着重要作用。

著录项

  • 作者

    Bley, Keith Roger.;

  • 作者单位

    Yale University.;

  • 授予单位 Yale University.;
  • 学科 Biology Neuroscience.
  • 学位 Ph.D.
  • 年度 2002
  • 页码 189 p.
  • 总页数 189
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 神经科学;
  • 关键词

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