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γ-氨基丁酸能抑制作用控制着下丘神经元中对双耳时间差敏感的神经增益。

GABAergic inhibition controls neural gain in inferior colliculus neurons sensitive to interaural time differences.

作者信息

Ingham Neil J, McAlpine David

机构信息

The Ear Institute and Department of Physiology, University College London, London WC1E 6BT, United Kingdom.

出版信息

J Neurosci. 2005 Jun 29;25(26):6187-98. doi: 10.1523/JNEUROSCI.0146-05.2005.

Abstract

We investigated the role of GABAergic inhibition on the responses of inferior colliculus (IC) neurons sensitive to interaural time differences (ITDs) in anesthetized guinea pigs. Responses to static and dynamic ITDs were obtained before, during, and after recovery from ionotophoretic application of GABA, or antagonists to the GABA(A) receptor gabazine and bicuculline. For most neurons, a linear relationship was observed between discharge rates evoked by a particular ITD during drug application and control discharge rates. Blocking GABAergic inhibition, or adding exogenous GABA, scaled IC discharge rates in a multiplicative (divisive) and/or additive (subtractive) manner. When the influence of iontophoresed GABA antagonists or exogenous GABA on discharge rates was accounted for, GABAergic inhibition was found to have no effect on the ITD tuning properties of IC neurons. The tuning sharpness of ITD functions, the ITD that evoked 50% response magnitude, and the relative symmetry of ITD functions around their peak response were unaffected by blockade of inhibition or addition of tonic inhibition. However, the ability of neurons to discriminate between ITDs by virtue of differences in their discharge rate was altered by blocking or adding GABA. We propose that inhibition in the IC is involved in the control of the neural gain of the output of IC neurons rather than the regulation of ITD tuning. This gain control appears to arise from a combination of additive and multiplicative processes, and may involve mechanisms such as shunting inhibition or changes in the efficacy of inhibitory and excitatory inputs.

摘要

我们研究了γ-氨基丁酸(GABA)能抑制对麻醉豚鼠下丘(IC)中对耳间时间差(ITD)敏感的神经元反应的作用。在离子电渗法施加GABA、GABA A受体拮抗剂荷包牡丹碱和荷包牡丹碱之前、期间和恢复后,获得了对静态和动态ITD的反应。对于大多数神经元,在药物应用期间特定ITD诱发的放电率与对照放电率之间观察到线性关系。阻断GABA能抑制或添加外源性GABA,以乘法(除法)和/或加法(减法)方式缩放IC放电率。当考虑离子电渗GABA拮抗剂或外源性GABA对放电率的影响时,发现GABA能抑制对IC神经元的ITD调谐特性没有影响。ITD功能的调谐锐度、诱发50%反应幅度的ITD以及ITD功能围绕其峰值反应的相对对称性不受抑制阻断或添加强直抑制的影响。然而,通过阻断或添加GABA,神经元凭借其放电率差异区分ITD的能力发生了改变。我们提出,IC中的抑制参与了IC神经元输出的神经增益控制,而不是ITD调谐的调节。这种增益控制似乎源于加法和乘法过程的组合,可能涉及诸如分流抑制或抑制性和兴奋性输入功效变化等机制。

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