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在猫中控制前庭眼震的抑制性爆发神经元(IBNs)上抑制性突触输入的神经递质。

The neurotransmitter of inhibitory synaptic inputs on inhibitory burst neurons (IBNs) controlling vestibular nystagmus in the cat.

作者信息

Yabe T, Furuya N

机构信息

Department of Otorhinolaryngology, Teikyo University School of Medicine, Tokyo, Japan.

出版信息

Acta Otolaryngol. 1993 Jan;113(1):11-7. doi: 10.3109/00016489309135760.

DOI:10.3109/00016489309135760
PMID:8095121
Abstract

In the pontine neural networks that govern vestibular nystagmus in the cat, inhibitory burst neurons (IBNs) are known to fire in bursts during the quick phase, and to suppress firing of the abducens motoneurons on the contralateral side. The present experiments were designed to identify the neurotransmitter controlling the burst firing pattern of IBNs. Inhibitory burst neuron activity was recorded extracellularly, and various chemicals were applied to the IBNs iontophoretically through multibarrel micropipettes. GABA and muscimol (a GABAA-receptor agonist) strongly suppressed IBN activity and eliminated the burst pattern. Bicuculline (a GABAA-receptor antagonist) increased the firing of IBNs and suppressed the inhibitory effect of GABA when applied simultaneously. Although baclofen (a GABAB-receptor agonist) had no inhibitory effect, it slightly shortened the duration of burst firing. Neither glycine nor serotonin, other inhibitory transmitter candidates, nor their respective antagonists, strychnine and methysergide, had any effect. Systemically administered picrotoxin prevented the GABA-induced suppression of IBNs. These results suggest that IBNs possess GABAA receptors and are controlled by higher GABA-liberating neurons and Cl- channels.

摘要

在猫中控制前庭眼震的脑桥神经网络中,已知抑制性爆发神经元(IBNs)在快速相期间会爆发式放电,并抑制对侧展神经运动神经元的放电。本实验旨在确定控制IBNs爆发式放电模式的神经递质。通过多管微电极细胞外记录抑制性爆发神经元的活动,并通过多管微电极将各种化学物质离子导入IBNs。γ-氨基丁酸(GABA)和蝇蕈醇(一种GABAA受体激动剂)强烈抑制IBNs的活动并消除爆发模式。荷包牡丹碱(一种GABAA受体拮抗剂)增加IBNs的放电,并在同时应用时抑制GABA的抑制作用。尽管巴氯芬(一种GABAB受体激动剂)没有抑制作用,但它略微缩短了爆发式放电的持续时间。甘氨酸和5-羟色胺(其他抑制性神经递质候选物)及其各自的拮抗剂士的宁和甲基麦角新碱均无任何作用。全身给予印防己毒素可防止GABA诱导的IBNs抑制。这些结果表明,IBNs具有GABAA受体,并受释放GABA的高级神经元和氯离子通道的控制。

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