跳转至内容
Merck
CN
  • Huntingtin recruits KIF1A to transport synaptic vesicle precursors along the mouse axon to support synaptic transmission and motor skill learning.

Huntingtin recruits KIF1A to transport synaptic vesicle precursors along the mouse axon to support synaptic transmission and motor skill learning.

eLife (2023-07-11)
Hélène Vitet, Julie Bruyère, Hao Xu, Claire Séris, Jacques Brocard, Yah-Sé Abada, Benoît Delatour, Chiara Scaramuzzino, Laurent Venance, Frédéric Saudou
摘要

Neurotransmitters are released at synapses by synaptic vesicles (SVs), which originate from SV precursors (SVPs) that have traveled along the axon. Because each synapse maintains a pool of SVs, only a small fraction of which are released, it has been thought that axonal transport of SVPs does not affect synaptic function. Here, studying the corticostriatal network both in microfluidic devices and in mice, we find that phosphorylation of the Huntingtin protein (HTT) increases axonal transport of SVPs and synaptic glutamate release by recruiting the kinesin motor KIF1A. In mice, constitutive HTT phosphorylation causes SV over-accumulation at synapses, increases the probability of SV release, and impairs motor skill learning on the rotating rod. Silencing KIF1A in these mice restored SV transport and motor skill learning to wild-type levels. Axonal SVP transport within the corticostriatal network thus influences synaptic plasticity and motor skill learning.

材料
产品编号
品牌
产品描述

Sigma-Aldrich
黏着斑蛋白单克隆抗体 小鼠抗, clone hVIN-1, ascites fluid
Sigma-Aldrich
抗 α-微管蛋白单克隆抗体 小鼠抗, clone DM1A, ascites fluid
Sigma-Aldrich
抗亨廷顿蛋白抗体,a.a.181-810,克隆 1HU-4C8, ascites fluid, clone 1HU-4C8, Chemicon®
Sigma-Aldrich
亨廷顿蛋白磷酸化Ser421抗体, Chemicon®, from rabbit