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神经激肽A通过抑制钾离子电导使牛蛙背根神经节的神经元去极化。

Neurokinin A depolarizes neurons of bullfrog dorsal root ganglia by suppressing K+ conductances.

作者信息

Akasu T, Ishimatsu M

机构信息

Department of Physiology, Kurume University School of Medicine, Japan.

出版信息

Kurume Med J. 1995;42(3):167-76. doi: 10.2739/kurumemedj.42.167.

Abstract

The effect of neurokinin A (NKA) on neurons of bullfrog dorsal root ganglia (DRG) in primary culture was examined by using whole-cell patch-clamp methods. Application of NKA (1 microM) depolarized the DRG neurons, resulting in spontaneous firing of action potentials. Under voltage-clamp condition, NKA (3 nM-1 microM) caused an inward current (INKA) associated with decreased membrane conductance. The INKA reversed its polarity at the equilibrium potential for K+. The INKA was blocked by extracellular Ba2+ (1 mM) but not by nominally 0 mM Ca2+, tetraethylammonium (40 mM), 4-aminopyridine (2 mM) or apamin (50 nM). Intracellular Cs+ blocked the INKA. NKA depressed a voltage-dependent non-inactivating K+ current, the M-current (IM), at potentials more positive than -55mV. NKA reduced the maximum M-conductance (GM) without changing the kinetics of M-channels. NKA also depressed a voltage- and time-independent background K+ current, IK(B). It is concluded that the INKA is produced by suppression of both IM and IK(B) in bullfrog primary afferent neurons.

摘要

采用全细胞膜片钳技术,研究了神经激肽A(NKA)对原代培养的牛蛙背根神经节(DRG)神经元的作用。施加NKA(1微摩尔)使DRG神经元去极化,导致动作电位的自发放电。在电压钳条件下,NKA(3纳摩尔 - 1微摩尔)引起内向电流(INKA),伴有膜电导降低。INKA在K + 的平衡电位处反转其极性。INKA可被细胞外Ba2 +(1毫摩尔)阻断,但不受名义上0毫摩尔的Ca2 +、四乙铵(40毫摩尔)、4 - 氨基吡啶(2毫摩尔)或蜂毒明肽(50纳摩尔)阻断。细胞内Cs + 阻断INKA。在电位高于 - 55毫伏时,NKA抑制电压依赖性非失活K + 电流,即M电流(IM)。NKA降低了最大M电导(GM),而不改变M通道的动力学。NKA还抑制了电压和时间依赖性的背景K + 电流IK(B)。得出的结论是,INKA是通过抑制牛蛙初级传入神经元中的IM和IK(B)产生的。

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