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蛙嗅球中气味诱导活动的γ-氨基丁酸能控制:用印防己毒素和荷包牡丹碱进行的电生理研究

GABAergic control of odor-induced activity in the frog olfactory bulb: electrophysiological study with picrotoxin and bicuculline.

作者信息

Duchamp-Viret P, Duchamp A, Chaput M

机构信息

Laboratoire de Physiologie Neurosensorielle, Université Claude-Bernard, Villeurbanne, France.

出版信息

Neuroscience. 1993 Mar;53(1):111-20. doi: 10.1016/0306-4522(93)90289-r.

DOI:10.1016/0306-4522(93)90289-r
PMID:8469302
Abstract

In the olfactory bulb, the first relay of the olfactory pathways, GABA, could be largely involved in the information processing since the two main populations of interneurons, periglomerular and granular cells, use it as neurotransmitter through reciprocal synapses with second-order neurons. This study planned to clarify the role of GABAergic inhibition in odor coding and, more precisely, the role of glomerular GABAergic inhibition. To do so, we attempted to specifically block in vivo GABAA receptors with either picrotoxin or bicuculline. The drug was applied at the level of the glomerular layer so that the antagonist could act primarily via periglomerular cells. The analysis of the effects of blocking GABAA on the coding was studied by recording the second-order neuron responses to odor stimuli delivered in a wide concentration range. Under drug treatment, the second-order neuron properties were deeply changed: response thresholds to odors were often lowered and spike bursts were more sustained in frequency and in duration. Thus, the GABAergic control on second-order neurons might be carried out by limiting the neuron excitability. GABAA antagonists applied in this manner could act to suppress the inhibitory effect of either the periglomerular cells or of the granule cells, both of which have been shown to contain enzymes for GABA production. The placement of the drug suggests to us that the action is primarily at the glomerulus. The results are consistent with periglomerular cells exerting a tonic inhibition on second-order neurons, an inhibition whose strength would be modulated by stimulus intensity. As a result, the amplifying role of glomerular convergence might be partly counterbalanced by input inhibition. Nevertheless, due to our procedure of drug application, one cannot rule out the possibility that the effects observed may partly reflect granular cell blocking. It can be concluded that the whole GABAergic inhibition, through GABAA receptors, permits a wide dynamic range of intensity coding.

摘要

在嗅球这个嗅觉通路的第一级中继站中,γ-氨基丁酸(GABA)可能在很大程度上参与信息处理,因为两类主要的中间神经元,即球周细胞和颗粒细胞,通过与二级神经元的相互突触将其用作神经递质。本研究旨在阐明GABA能抑制在气味编码中的作用,更确切地说是肾小球GABA能抑制的作用。为此,我们试图用印防己毒素或荷包牡丹碱在体内特异性阻断GABAA受体。药物在肾小球层水平施用,以便拮抗剂主要通过球周细胞起作用。通过记录二级神经元对在很宽浓度范围内传递的气味刺激的反应,研究了阻断GABAA对编码的影响。在药物治疗下,二级神经元特性发生了深刻变化:对气味的反应阈值常常降低,且动作电位爆发在频率和持续时间上更持久。因此,对二级神经元的GABA能控制可能是通过限制神经元兴奋性来实现的。以这种方式施用的GABAA拮抗剂可能会抑制球周细胞或颗粒细胞的抑制作用,这两类细胞均已被证明含有GABA生成酶。药物的施用部位向我们表明其作用主要发生在肾小球。结果与球周细胞对二级神经元施加紧张性抑制一致,这种抑制的强度会受到刺激强度的调节。因此,肾小球汇聚的放大作用可能会被输入抑制部分抵消。然而,由于我们的药物施用程序,不能排除观察到的效应可能部分反映颗粒细胞被阻断的可能性。可以得出结论,通过GABAA受体的整个GABA能抑制允许强度编码有很宽的动态范围。

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