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致聋后鸟类发声运动皮层中树突棘的重塑依赖于基底神经节回路。

Remodeling of Dendritic Spines in the Avian Vocal Motor Cortex Following Deafening Depends on the Basal Ganglia Circuit.

作者信息

Zhou Xin, Fu Xin, Lin Chun, Zhou Xiaojuan, Liu Jin, Wang Li, Zhang Xinwen, Zuo Mingxue, Fan Xiaolong, Li Dapeng, Sun Yingyu

机构信息

Beijing Key Laboratory of Gene Resource and Molecular Development, Laboratory of Neuroscience and Brain Development, College of Life Sciences, Beijing Normal University, Beijing 100875, China.

Department of Biology, Hainan Normal University, Haikou 571158, China.

出版信息

Cereb Cortex. 2017 May 1;27(5):2820-2830. doi: 10.1093/cercor/bhw130.

Abstract

Deafening elicits a deterioration of learned vocalization, in both humans and songbirds. In songbirds, learned vocal plasticity has been shown to depend on the basal ganglia-cortical circuit, but the underlying cellular basis remains to be clarified. Using confocal imaging and electron microscopy, we examined the effect of deafening on dendritic spines in avian vocal motor cortex, the robust nucleus of the arcopallium (RA), and investigated the role of the basal ganglia circuit in motor cortex plasticity. We found rapid structural changes to RA dendritic spines in response to hearing loss, accompanied by learned song degradation. In particular, the morphological characters of RA spine synaptic contacts between 2 major pathways were altered differently. However, experimental disruption of the basal ganglia circuit, through lesions in song-specialized basal ganglia nucleus Area X, largely prevented both the observed changes to RA dendritic spines and the song deterioration after hearing loss. Our results provide cellular evidence to highlight a key role of the basal ganglia circuit in the motor cortical plasticity that underlies learned vocal plasticity.

摘要

在人类和鸣禽中,致聋都会引发习得发声能力的退化。在鸣禽中,已证明习得的发声可塑性依赖于基底神经节 - 皮质回路,但其潜在的细胞基础仍有待阐明。我们使用共聚焦成像和电子显微镜,研究了致聋对鸟类发声运动皮层、弓状皮质粗壮核(RA)中树突棘的影响,并探讨了基底神经节回路在运动皮层可塑性中的作用。我们发现,听力丧失会使RA树突棘发生快速的结构变化,并伴有习得鸣叫的退化。特别是,两条主要通路之间RA棘突突触接触的形态特征发生了不同的改变。然而,通过损毁鸣禽特化的基底神经节核团X区来实验性破坏基底神经节回路,在很大程度上阻止了观察到的RA树突棘变化以及听力丧失后的鸣叫退化。我们的研究结果提供了细胞层面的证据,以突出基底神经节回路在作为习得发声可塑性基础的运动皮层可塑性中的关键作用。

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