NEUROTRANSMITTERS DECREASE THE CALCIUM CONDUCTANCE ACTIVATED BY DEPOLARIZATION OF EMBRYONIC CHICK SENSORY NEURONS
NEUROTRANSMITTERS DECREASE THE CALCIUM CONDUCTANCE ACTIVATED BY DEPOLARIZATION OF EMBRYONIC CHICK SENSORY NEURONS
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DOI：
10.1113/jphysiol.1981.sp013841
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发表时间：
1981-01-01
影响因子：
5.5
通讯作者：
FISCHBACH, GD
中科院分区：
文献类型：
--
作者：
DUNLAP, K;FISCHBACH, GD
几种神经递质，包括去甲肾上腺素（NA），GABA和5-羟色胺（5-HT），和某些肽减少记录在细胞培养的胚胎鸡背根神经节神经元胞体中的Na+-Ca 2+动作电位的持续时间。为了确定这些药物是否通过影响Ca 2+通道（内向电流）或K+通道（外向电流）来降低动作电位持续时间，在电压钳位感觉神经元胞体中记录膜电流。去极化产生了一个突出的内向Na+电流和一个较小的和缓慢的内向Ca 2+电流（伊卡）。伊卡的失活不仅依赖于膜电位，而且显然需要预先进入Ca ~（2+）。两个组件的外向电流，电压激活和Ca 2+激活，在大多数细胞中是显而易见的。NA以及GABA和5-HT的作用源自对伊卡的直接作用，因为NA降低了在EK处记录的TTX[河豚毒素]抗性尾电流以及在125 mM-TEA和TTX存在下记录的内向电流（其中Na+和K+电流被阻断）。伊卡的减少最有可能是由于对可用的Ca 2+通道的数量和/或单个Ca 2+通道电导的影响，而不是由于通道激活动力学或Ca 2+平衡电位的变化。几种递质对电压依赖性Na+和K+电流无影响。伊卡调制的突触前抑制现象的影响进行了讨论。
Several neurotransmitters including noradrenaline [norepinephrine] (NA), GABA and serotonin [5-hydroxytryptamine] (5-HT), and certain peptides decrease the duration of the Na+-Ca2+ action potential recorded in cell bodies of embryonic chick dorsal root ganglion neurons maintained in cell culture. To determine if these agents decreased action potential duration by affecting Ca2+ channels (inward current) or K+ channels (outward current) membrane currents were recorded in voltage-clamped sensory neuron somata. Depolarization produced a prominent inward Na+ current and a smaller and slower inward Ca2+ current (ICa). The inactivation of ICa was not simply dependent on membrane potential but apparently required prior entry of Ca2+. Two components of outward current, voltage-activated and Ca2+-activated, were evident in most cells. The effect of NA, and also of GABA and 5-HT, resulted from a direct effect on ICa because NA decreased the TTX[tetrodotoxin]-resistant tail current recorded at EK and the inward current recorded in the presence of 125 mM-TEA and TTX (in which Na+ and K+ currents were blocked). The decrease in ICa is most likely due to an effect on the number of available Ca2+ channels and/or the single Ca2+ channel conductance rather than to a shift in either the kinetics of channel activation or the Ca2+ equilibrium potential. No effect of the several transmitters on the voltage-dependent Na+ and K+ currents was observed. Implications of ICa modulation for the phenomenon of presynaptic inhibition are discussed.