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帕金森病小鼠模型中神经振荡的短暂增加和运动缺陷。

Transient Increases in Neural Oscillations and Motor Deficits in a Mouse Model of Parkinson's Disease.

机构信息

Key Laboratory of Southwest China Wildlife Resources Conservation (Ministry of Education), China West Normal University, Nanchong 637009, China.

Chengdu Institute of Biology, Chinese Academy of Sciences, Chengdu 610213, China.

出版信息

Int J Mol Sci. 2024 Sep 2;25(17):9545. doi: 10.3390/ijms25179545.

Abstract

Parkinson's disease (PD) is a neurodegenerative disorder characterized by motor symptoms like tremors and bradykinesia. PD's pathology involves the aggregation of α-synuclein and loss of dopaminergic neurons, leading to altered neural oscillations in the cortico-basal ganglia-thalamic network. Despite extensive research, the relationship between the motor symptoms of PD and transient changes in brain oscillations before and after motor tasks in different brain regions remain unclear. This study aimed to investigate neural oscillations in both healthy and PD model mice using local field potential (LFP) recordings from multiple brain regions during rest and locomotion. The histological evaluation confirmed the significant dopaminergic neuron loss in the injection side in 6-OHDA lesioned mice. Behavioral tests showed motor deficits in these mice, including impaired coordination and increased forelimb asymmetry. The LFP analysis revealed increased delta, theta, alpha, beta, and gamma band activity in 6-OHDA lesioned mice during movement, with significant increases in multiple brain regions, including the primary motor cortex (M1), caudate-putamen (CPu), subthalamic nucleus (STN), substantia nigra pars compacta (SNc), and pedunculopontine nucleus (PPN). Taken together, these results show that the motor symptoms of PD are accompanied by significant transient increases in brain oscillations, especially in the gamma band. This study provides potential biomarkers for early diagnosis and therapeutic evaluation by elucidating the relationship between specific neural oscillations and motor deficits in PD.

摘要

帕金森病(PD)是一种神经退行性疾病,其特征为震颤和运动徐缓等运动症状。PD 的病理学涉及α-突触核蛋白的聚集和多巴胺能神经元的丧失,导致皮质基底节丘脑网络中的神经振荡改变。尽管进行了广泛的研究,但 PD 患者在进行运动任务前后不同脑区脑振荡的短暂变化与运动症状之间的关系仍不清楚。本研究旨在使用局部场电位(LFP)记录,研究健康和 PD 模型小鼠在休息和运动期间来自多个脑区的神经振荡。组织学评估证实,6-OHDA 损伤的小鼠在注射侧的多巴胺能神经元显著丧失。行为测试显示这些小鼠存在运动缺陷,包括协调能力受损和前肢不对称性增加。LFP 分析显示,6-OHDA 损伤的小鼠在运动期间的 delta、theta、alpha、beta 和 gamma 波段活动增加,多个脑区的活动显著增加,包括初级运动皮层(M1)、尾壳核(CPu)、丘脑底核(STN)、黑质致密部(SNc)和脑桥被盖核(PPN)。综上所述,这些结果表明,PD 的运动症状伴随着脑振荡的显著短暂增加,尤其是在 gamma 波段。本研究通过阐明 PD 中特定神经振荡与运动缺陷之间的关系,为早期诊断和治疗评估提供了潜在的生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/060c/11394686/af7b203f0326/ijms-25-09545-g001.jpg

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