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胡须经验调节桶状皮层中γ-氨基丁酸能中间神经元的长时程抑郁。

Whisker experience modulates long-term depression in neocortical γ-aminobutyric acidergic interneurons in barrel cortex.

机构信息

Department of Zoology and Physiology, University of Wyoming, Laramie, Wyoming 82071, USA.

出版信息

J Neurosci Res. 2011 Jan;89(1):73-85. doi: 10.1002/jnr.22530.

Abstract

Long-term plasticity is believed to be an important mechanism that allows neural circuits to be modulated in an use-dependent manner. However, evidence regarding the role of sensory experience in modulating long-term plasticity of glutamatergic synapses in neocortical GABAergic interneurons is unavailable. Here, we focused on regular-spiking nonpyramidal (RSNP) interneurons and examined spike-pairing-induced plasticity of glutamatergic synapses and its modulation by sensory experiences ex vivo. In our previous studies, RSNP interneurons do not show experience-dependent plasticity of intrinsic properties or alteration of thalamocortical (TC) synapses and exhibit robust modulation by mGluRs. Here we report a spike-pairing-induced long-term depression (spLTD) of glutamatergic synapses in RSNP interneurons of barrels cortex. Using paired recording and thalamic-induced responses, we found that the spLTD was specific for intracortical but not TC synapses. The spLTD was mediated via presynaptic mGluRs. The spLTD was not modulated by chronic or acute administration of NMDAR antagonists but was enhanced by sensory deprivation (via whisker trimming) during a postnatal sensitive period ex vivo. The synapses specific spLTD to intracortical glutamatergic synapses in RSNP cells and their modulation by sensory deprivation may contribute to sensory-dependent remodeling of cortical circuits and redistribution circuit activity along the whisker-related columns.

摘要

长期可塑性被认为是一种重要的机制,允许神经回路以依赖使用的方式进行调节。然而,关于感觉经验在调节新皮层 GABA 能中间神经元谷氨酸能突触的长期可塑性中的作用的证据尚不清楚。在这里,我们专注于规则放电非锥体(RSNP)中间神经元,并在体外用尖峰对诱导的可塑性来检查谷氨酸能突触及其对感觉经验的调节。在我们之前的研究中,RSNP 中间神经元没有表现出对内在特性的经验依赖性可塑性或丘脑皮质(TC)突触的改变,并且对 mGluRs 表现出强大的调节作用。在这里,我们报告了 RSNP 中间神经元的桶状皮层中谷氨酸能突触的尖峰对诱导的长时程抑制(spLTD)。使用成对记录和丘脑诱导反应,我们发现 spLTD 是皮质内特有的,而不是 TC 突触。spLTD 通过突触前 mGluRs 介导。spLTD 不受慢性或急性 NMDAR 拮抗剂给药的调节,但在体外向敏感期(通过修剪胡须)剥夺感觉后增强。RSNP 细胞中皮质内谷氨酸能突触的特异性 spLTD 及其对感觉剥夺的调节可能有助于皮质回路的感觉依赖性重塑和沿胡须相关柱的回路活动的重新分布。

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