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小脑皮质兴奋性的局部变化会在复杂锋电位同步性上产生空间受限的变化。

Local changes in the excitability of the cerebellar cortex produce spatially restricted changes in complex spike synchrony.

作者信息

Marshall Sarah P, Lang Eric J

机构信息

Department of Physiology and Neuroscience, New York University School of Medicine, New York, New York 10016, USA.

出版信息

J Neurosci. 2009 Nov 11;29(45):14352-62. doi: 10.1523/JNEUROSCI.3498-09.2009.

DOI:10.1523/JNEUROSCI.3498-09.2009
PMID:19906982
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2834270/
Abstract

Complex spike (CS) synchrony patterns are modulated by the release of GABA within the inferior olive (IO). The GABAergic projection to most of the IO arises from the cerebellar nuclei, which are themselves subject to strong inhibitory control by Purkinje cells in the overlying cortex. Moreover, the connections between the IO and cerebellum are precisely aligned, raising the possibility that each cortical region controls its own CS synchrony distribution. This possibility was tested using multielectrode recordings of CSs and simple spikes (SSs) in crus 2a of anesthetized rats. Picrotoxin or muscimol was applied to the cerebellar cortex at the borders of the recording array. These drugs induced significant changes in CS synchrony and in CS and SS firing rates and changes in post-CS pauses and modulation of SS activity. The level of CS synchrony was correlated with SS firing rate in control, and application of picrotoxin increased both. In contrast, muscimol decreased CS synchrony. Furthermore, when picrotoxin was applied only at the lateral edge of the array, changes in CS synchrony occurred sequentially across the recording array, with cells located in the lateral half of the array having earlier and larger changes in CS synchrony than cells in the medial half. The results indicate that a double-inhibitory feedback circuit from Purkinje cells to the IO provides a mechanism by which SS activity may regulate CS synchrony. Thus, CS synchrony may be a physiologically controlled parameter of cerebellar activity, with the cerebellum and IO comprising a series of self-updating circuits.

摘要

复杂峰电位(CS)同步模式受下橄榄核(IO)内γ-氨基丁酸(GABA)释放的调节。向大部分IO的GABA能投射起源于小脑核,而小脑核本身受到覆盖皮质中浦肯野细胞的强烈抑制控制。此外,IO和小脑之间的连接精确对齐,这增加了每个皮质区域控制其自身CS同步分布的可能性。使用麻醉大鼠2a腿部的CS和简单峰电位(SS)的多电极记录来测试这种可能性。将印防己毒素或蝇蕈醇应用于记录阵列边界处的小脑皮质。这些药物引起CS同步性、CS和SS放电率的显著变化,以及CS后停顿和SS活动调制的变化。在对照中,CS同步水平与SS放电率相关,印防己毒素的应用增加了两者。相比之下,蝇蕈醇降低了CS同步性。此外,当仅在阵列的外侧边缘应用印防己毒素时,CS同步性的变化在整个记录阵列中依次发生,位于阵列外侧一半的细胞比内侧一半的细胞在CS同步性上有更早、更大的变化。结果表明,从浦肯野细胞到IO的双抑制反馈回路提供了一种机制,通过该机制SS活动可以调节CS同步性。因此,CS同步性可能是小脑活动的一个生理控制参数,小脑和IO构成了一系列自我更新的回路。

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