GABA_A和GABA_B受体介导的蟾蜍背根神经节神经元胞体膜反应

实验在蟾蜍离体背根神经节(DRG)标本进行细胞内记录。浴槽滴加10~(-4)-10~(-3)mol/LGABA引起膜电位改变如下:(1)去极化(79/100);(2)双相反应;先为去极化,继后为超极化(10/100);(3)无反应(11/100)。以上去极化反应均可为荷包牡丹碱所阻断。GABA-去极化时膜电导增加,逆转电位值为-15——25mV。低Cl~-和高Cl~-任氏液分别使GABA-去极化反应增大和减小。10~(-4)mol/Lbaclofen不引起膜电位改变。在GABA-去极化期间,观察到大部分细胞的动作电位时程(ApD)缩短。ApD的此种变化可为baclofen所模拟,但不为荷包牡丹碱所阻断。结果提示:蟾蜍DRG神经元胞体膜有GABA_A和GABA_B受体共存,前者介导膜电位的改变,后者介导ApD的缩短。本文并联系到初级传入终末的突触前抑制的产生机制进行了讨论。

RESPONSES MEDIATED BY GABA_A AND GABA_B RECEPTORS ON THE SOMATIC MEMBRANE OF TOAD DORSAL ROOT GANGLION NEURONES

Intracellular recordings were made from neurons in toad dorsal root ganglion invitro. Bath application of GABA (10~(-4)--10~(-3) mol/L) elicited either depolarization ordepolarization followed by hyperpolarization respectively in 79% and 10% of the neu-rons. The remaining 11% did not show any response. Th. GABA--induced depolariza-tion, which was accompanied by an increase of membrane conductance and usually ashortening of action potential duration (ApD), could be blocked by bicuculline. TheGABA--depolarization was enhanced by low Cl~- Ringer or reduced by high Cl~-Ringer. The membrane potential was not affected by 10~(-4) mol/L baclofen. On theother hand, shortening of ApD could be produced by baclofen, but not blocked bybicuculline. Our results suggested that GABA_A and GABA_B receptors coexist on the so-matic membrane of toad dorsal root ganglion neurons and mediate the changes respec-tively in membrane potential and shortening of ApD. The mechanism underlyingpresynaptic inhibition in the terminals of the primary afferents was discussed.