Neuronal activity pattern defects in the striatum in awake mouse model of Parkinson's disease

被引:15
|
作者
Chen, Hui [1 ]
Lei, Huimeng [1 ]
Xu, Qunyuan [1 ]
机构
[1] Capital Med Univ, Beijing Inst Brain Disorders, Key Lab Neurodegenerat Dis,Minist Educ, Beijing Ctr Neural Regenerat & Repair,Dept Neurob, Beijing 100069, Peoples R China
基金
中国国家自然科学基金;
关键词
Parkinson's disease; 6-OHDA mouse model; Dopamine; Movement; striatum; Electrophysiology; FAST-SPIKING INTERNEURONS; BASAL GANGLIA OUTPUT; DEEP BRAIN-STIMULATION; BETA-BAND OSCILLATIONS; SUBTHALAMIC NUCLEUS; PROJECTION NEURONS; GABAERGIC INTERNEURONS; DOPAMINE DEPLETION; 6-OHDA LESION; MOTOR CORTEX;
D O I
10.1016/j.bbr.2017.12.018
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
Previous studies showed the loss of dopaminergic neurons directly leads to both changes in firing rate and neuronal synchrony in the striatum by pharmacogenetic approach, but physiological observation of striatal neurons in awake animal is rare up to now due to the limitation of recording methods. We use multichannel in vivo recording system, to record the activity pattern of both medium spiny projecting neurons (MSNs) and fast spiking interneurons (FSIs) in awake mouse model of Parkinson's disease (PD), created by injection of 6-hydroxyl-dopamine (6-OHDA) into dorsolateral striatum bilaterally and unilaterally. The abnormal discharge of neurons, including oscillations, burst activity and firing rate were systematically observed, and we used these index together to comprehensively analyse the functional change of striatal neurons in PD mouse model. We found that PD mouse model exhibited elevated synchronized oscillatory activity in beta frequency band and decreased firing rate of FSIs during movement. The firing rate and burst activity of MSNs clearly reduced during movement after bilateral dopamine depletion. The present study has novelly shown the firing pattern changes of the MSNs and FSIs in DL striatum in awake PD mouse model, by combination of electrophysiology with molecular biological technology. Our results may help to reveal a new circuitry mechanism of movement disorders in PD.
引用
收藏
页码:135 / 145
页数:11
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