Akasu T, Ishimatsu M
Department of Physiology, Kurume University School of Medicine, Japan.
Kurume Med J. 1995;42(3):167-76. doi: 10.2739/kurumemedj.42.167.
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.
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。
