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大鼠下丘中GABA(B)受体对GABA能抑制的突触前调制

Presynaptic modulation of GABAergic inhibition by GABA(B) receptors in the rat's inferior colliculus.

作者信息

Ma C L, Kelly J B, Wu S H

机构信息

Laboratory of Sensory Neuroscience, Psychology Department, 335 Life Sciences Research Building, Carleton University, 1125 Colonel By Drive, K1S 5B6, Ottawa, ON, Canada

出版信息

Neuroscience. 2002;114(1):207-15. doi: 10.1016/s0306-4522(02)00130-6.

Abstract

Whole-cell patch clamp recordings were made from neurons in a brain slice preparation of the inferior colliculus in 11-15-day-old rat pups. Synaptic responses were elicited by applying a current pulse to the lateral lemniscus just below the central nucleus of the inferior colliculus. To examine GABAergic inhibition in the inferior colliculus all excitatory postsynaptic potentials and glycinergic inhibitory postsynaptic potentials were blocked by bath application of their respective antagonists and the contribution of GABA(B) receptors was determined for the remaining inhibitory postsynaptic potentials. For most cells the isolated inhibitory postsynaptic potential was completely blocked by the GABA(A) receptor antagonist, bicuculline, but was unaffected by the GABA(B) receptor antagonist, phaclofen. The GABA(B) receptor agonist, baclofen (10-20 microM), decreased the amplitude of the inhibitory postsynaptic potentials. This effect was completely blocked by phaclofen. Baclofen did not increase the cell membrane conductance or alter the rate of firing produced by depolarization of the cell membrane. In contrast, muscimol, a GABA(A) receptor agonist, greatly increased membrane conductance and lowered the firing rate produced by depolarization. Our results indicate that GABAergic inhibition in the auditory midbrain can be reduced by the activation of GABA(B) receptors and suggest that the effects are presynaptic.

摘要

采用全细胞膜片钳记录技术,对11 - 15日龄幼鼠下丘脑片制备中的神经元进行记录。通过向下丘中央核下方的外侧丘系施加电流脉冲来诱发突触反应。为了研究下丘中的GABA能抑制作用,通过浴灌各自的拮抗剂来阻断所有兴奋性突触后电位和甘氨酸能抑制性突触后电位,并确定GABA(B)受体对剩余抑制性突触后电位的作用。对于大多数细胞,分离出的抑制性突触后电位被GABA(A)受体拮抗剂荷包牡丹碱完全阻断,但不受GABA(B)受体拮抗剂巴氯芬的影响。GABA(B)受体激动剂巴氯芬(10 - 20微摩尔)降低了抑制性突触后电位的幅度。这种作用被巴氯芬完全阻断。巴氯芬没有增加细胞膜电导,也没有改变细胞膜去极化产生的放电频率。相比之下,GABA(A)受体激动剂蝇蕈醇极大地增加了膜电导并降低了去极化产生的放电频率。我们的结果表明,听觉中脑中的GABA能抑制作用可通过GABA(B)受体的激活而降低,并提示其作用是突触前的。

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