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氯离子电导在初级传入神经中产生突触前抑制和逆向峰电位。

Chloride conductance produces both presynaptic inhibition and antidromic spikes in primary afferents.

作者信息

Cattaert D, el Manira A, Clarac F

机构信息

Laboratoire Neurobiologie et Mouvements, CNRS, Marseille, France.

出版信息

Brain Res. 1994 Dec 12;666(1):109-12. doi: 10.1016/0006-8993(94)90289-5.

DOI:10.1016/0006-8993(94)90289-5
PMID:7889358
Abstract

Primary afferents from a crayfish leg proprioceptor display both primary afferent depolarizations (PADs) and antidromic spikes. PADs are generated by activation of GABA receptors and produce presynaptic inhibition, while the antidromic spikes do not elicit any synaptic effect in the postsynaptic neurons. The aim of the present study was to investigate the ionic mechanisms that allow PADs to produce antidromic spikes and to test whether GABA can produce similar effects. Intracellular recordings from the sensory axon terminals within the ganglion where PAD are produced were performed. Lowering the extracellular chloride concentration resulted in an increase in PAD amplitude, which was then capable of producing antidromic spikes. Local application of GABA close to the axon terminal also resulted in production of antidromic spikes. We conclude that antidromic spikes may result from the activation of a GABA-mediated increase in chloride conductance that also produces PADs. Therefore PADs and antidromic spikes may represent two aspects of the same GABAergic inhibitory mechanism that gate sensory transmission.

摘要

小龙虾腿部本体感受器的初级传入纤维表现出初级传入去极化(PADs)和逆向动作电位。PADs由GABA受体激活产生,并产生突触前抑制,而逆向动作电位在突触后神经元中不引发任何突触效应。本研究的目的是研究使PADs产生逆向动作电位的离子机制,并测试GABA是否能产生类似的效应。对产生PADs的神经节内感觉轴突终末进行了细胞内记录。降低细胞外氯离子浓度导致PADs幅度增加,进而能够产生逆向动作电位。在轴突终末附近局部应用GABA也导致逆向动作电位的产生。我们得出结论,逆向动作电位可能源于GABA介导的氯离子电导增加的激活,而这也会产生PADs。因此,PADs和逆向动作电位可能代表了同一GABA能抑制机制的两个方面,该机制控制着感觉传递。

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