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哺乳动物延髓呼吸神经元中的钙电流和钙依赖性钾电流。

Calcium currents and calcium-dependent potassium currents in mammalian medullary respiratory neurones.

作者信息

Richter D W, Champagnat J, Jacquin T, Benacka R

机构信息

II. Physiologisches Institut, Universität Göttingen, FRG.

出版信息

J Physiol. 1993 Oct;470:23-33. doi: 10.1113/jphysiol.1993.sp019844.

Abstract
  1. Respiratory neurons of mammals are rhythmically active because their membrane potential fluctuates periodically over a voltage range of -70 to -55 mV. These respiratory drive potentials lead to periodic discharges of bursts of action potentials lasting for 1-2 s. The neuronal processes stabilizing this rhythmic activity involve excitatory and inhibitory synaptic processes that interact with specific membrane properties of the postsynaptic neurones. In the present experiments, performed on dorsal and ventral groups of respiratory neurones under in vivo and in vitro conditions, we verified the modulating feature of such intrinsic neuronal properties. 2. Intrinsic neuronal properties involve Ca2+ mechanisms that lead to intracellular Ca2+ accumulation, and consequently to activation of Ca(2+)-dependent K+ currents. 3. Blockade of intracellular Ca2+ accumulation significantly changed the amplitude and pattern of respiratory drive potentials, and blocked initial hyperpolarizing shifts of the membrane potential following each period of synaptic activation. 4. The data demonstrate that postsynaptic activities and action potential discharges activate low and high voltage-activated Ca2+ currents leading to intracellular Ca2+ accumulation and to activation of Ca(2+)-dependent K+ currents that significantly modulate the voltage response of medullary respiratory neurones to on-going synaptic activation. These intrinsic membrane properties also seem to be involved in the processes controlling termination of rhythmic burst discharges.
摘要
  1. 哺乳动物的呼吸神经元有节律地活动,因为它们的膜电位在-70至-55 mV的电压范围内周期性波动。这些呼吸驱动电位导致持续1 - 2秒的动作电位爆发的周期性发放。稳定这种节律性活动的神经元过程涉及与突触后神经元特定膜特性相互作用的兴奋性和抑制性突触过程。在本实验中,我们在体内和体外条件下对呼吸神经元的背侧和腹侧组进行了实验,验证了这种内在神经元特性的调节特征。2. 内在神经元特性涉及导致细胞内Ca2+积累的Ca2+机制,进而导致Ca(2+)依赖性K+电流的激活。3. 细胞内Ca2+积累的阻断显著改变了呼吸驱动电位的幅度和模式,并阻断了每次突触激活期后膜电位的初始超极化转变。4. 数据表明,突触后活动和动作电位发放激活了低电压和高电压激活的Ca2+电流,导致细胞内Ca2+积累,并激活了Ca(2+)依赖性K+电流,这些电流显著调节延髓呼吸神经元对持续突触激活的电压反应。这些内在膜特性似乎也参与了控制节律性爆发发放终止的过程。

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本文引用的文献

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Mechanisms underlying post-inspiratory depolarization in post-inspiratory neurons of the cat.
Neurosci Lett. 1993 Feb 5;150(1):1-4. doi: 10.1016/0304-3940(93)90093-z.
2
Generation and maintenance of the respiratory rhythm.呼吸节律的产生与维持。
J Exp Biol. 1982 Oct;100:93-107. doi: 10.1242/jeb.100.1.93.
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The effects of QX-314 on medullary respiratory neurones.QX-314对延髓呼吸神经元的作用。
Brain Res. 1987 Sep 8;420(1):22-31. doi: 10.1016/0006-8993(87)90235-6.

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