Lin Z W, Li Z W
Research Centre of Experimental Medicine, Tongji Medical University, Wuhan.
Sheng Li Xue Bao. 1993 Apr;45(2):117-23.
Intracellular recordings were made from neurons in toad dorsal root ganglion in vitro. Bath application of GABA (10(-4)-10(-3) mol/L) elicited either depolarization or depolarization followed by hyperpolarization respectively in 79% and 10% of the neurons. The remaining 11% did not show any response. The GABA-induced depolarization, which was accompanied by an increase of membrane conductance and usually a shortening of action potential duration (ApD), could be blocked by bicuculline. The GABA-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 the other hand, shortening of ApD could be produced by baclofen, but not blocked by bicuculline. Our results suggested that GABAA and GABAB receptors coexist on the somatic membrane of toad dorsal root ganglion neurons and mediate the changes respectively in membrane potential and shortening of ApD. The mechanism underlying presynaptic inhibition in the terminals of the primary afferents was discussed.
在体外对蟾蜍背根神经节中的神经元进行细胞内记录。浴用γ-氨基丁酸(GABA,10⁻⁴ - 10⁻³mol/L)分别在79%和10%的神经元中引起去极化或先去极化后超极化。其余11%未表现出任何反应。GABA诱导的去极化伴有膜电导增加且通常动作电位时程(ApD)缩短,可被荷包牡丹碱阻断。低氯林格液增强GABA去极化,高氯林格液则使其减弱。10⁻⁴mol/L巴氯芬不影响膜电位。另一方面,巴氯芬可使ApD缩短,但不被荷包牡丹碱阻断。我们的结果表明,GABAA和GABAB受体共存于蟾蜍背根神经节神经元的胞体膜上,并分别介导膜电位变化和ApD缩短。文中还讨论了初级传入纤维终末突触前抑制的机制。