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树突棘和突触接触的稳定性由α N-连环蛋白控制。

Stability of dendritic spines and synaptic contacts is controlled by alpha N-catenin.

作者信息

Abe Kentaro, Chisaka Osamu, Van Roy Frans, Takeichi Masatoshi

机构信息

RIKEN Center for Developmental Biology, 2-2-3 Minatojima-Minamimachi, Chuo-ku, Kobe 650-0047, Japan.

出版信息

Nat Neurosci. 2004 Apr;7(4):357-63. doi: 10.1038/nn1212. Epub 2004 Mar 21.

DOI:10.1038/nn1212
PMID:15034585
Abstract

Morphological plasticity of dendritic spines and synapses is thought to be crucial for their physiological functions. Here we show that alpha N-catenin, a linker between cadherin adhesion receptors and the actin cytoskeleton, is essential for stabilizing dendritic spines in rodent hippocampal neurons in culture. In the absence of alpha N-catenin, spine heads were abnormally motile, actively protruding filopodia from their synaptic contact sites. Conversely, alpha N-catenin overexpression in dendrites reduced spine turnover, causing an increase in spine and synapse density. Tetrodotoxin (TTX), a neural activity blocker, suppressed the synaptic accumulation of alpha N-catenin, whereas bicuculline, a GABA antagonist, promoted it. Furthermore, excess alpha N-catenin rendered spines resistant to the TTX treatment. These results suggest that alpha N-catenin is a key regulator for the stability of synaptic contacts.

摘要

树突棘和突触的形态可塑性被认为对其生理功能至关重要。我们在此表明,αN-连环蛋白是一种钙黏蛋白黏附受体与肌动蛋白细胞骨架之间的连接蛋白,对于稳定培养的啮齿动物海马神经元中的树突棘至关重要。在缺乏αN-连环蛋白的情况下,棘头异常活跃,从其突触接触部位伸出活跃的丝状伪足。相反,树突中αN-连环蛋白的过表达减少了棘的更新,导致棘和突触密度增加。神经活动阻滞剂河豚毒素(TTX)抑制了αN-连环蛋白的突触积累,而GABA拮抗剂荷包牡丹碱则促进了它的积累。此外,过量的αN-连环蛋白使棘对TTX处理具有抗性。这些结果表明,αN-连环蛋白是突触接触稳定性的关键调节因子。

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