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浦肯野神经元突触钙调节机制的功能整合。

Functional integration of calcium regulatory mechanisms at Purkinje neuron synapses.

机构信息

Department of Physiology, Brain Health and Repair Research Centre, University of Otago School of Medical Sciences, Dunedin, New Zealand.

出版信息

Cerebellum. 2012 Sep;11(3):640-50. doi: 10.1007/s12311-010-0185-6.

Abstract

Cerebellar Purkinje neurons receive synaptic inputs from three different sources: the excitatory parallel fibre and climbing fibre synapses as well as the inhibitory synapses from molecular layer stellate and basket cells. These three synaptic systems use distinct mechanisms in order to generate Ca(2+) signals that are specialized for specific modes of neurotransmitter release and post-synaptic signal integration. In this review, we first describe the repertoire of Ca(2+) regulatory mechanisms that generate and regulate the amplitude and timing of Ca(2+) fluxes during synaptic transmission and then explore how these mechanisms interact to generate the unique functional properties of each of the Purkinje neuron synapses.

摘要

小脑浦肯野神经元接收来自三个不同来源的突触输入

兴奋性平行纤维和 climbing 纤维突触,以及来自分子层星状细胞和篮状细胞的抑制性突触。这三个突触系统使用不同的机制来产生 Ca(2+)信号,这些信号专门用于特定的神经递质释放和突触后信号整合模式。在这篇综述中,我们首先描述了产生和调节突触传递过程中 Ca(2+)流幅度和时程的 Ca(2+)调节机制的组合,然后探讨了这些机制如何相互作用,从而产生每个浦肯野神经元突触的独特功能特性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82a5/3411285/2cfbe2221a50/12311_2010_185_Fig1_HTML.jpg

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