Altered Thalamocortical Signaling in a Mouse Model of Parkinson's Disease

被引:7
作者
Swanson, Olivia K. [1 ,2 ]
Yevoo, Priscilla E. [1 ,2 ]
Richard, Dave [1 ]
Maffei, Arianna [1 ,2 ]
机构
[1] SUNY Stony Brook, Dept Neurobiol & Behav, Stony Brook, NY 11794 USA
[2] SUNY Stony Brook, Grad Program Neurosci, Stony Brook, NY 11794 USA
关键词
dopamine; Parkinson's disease; parvalbumin; pyramidal neuron; synaptic transmission; thalamocortical; MOTOR CORTEX; GABAERGIC INTERNEURONS; INHIBITORY CIRCUITS; PROJECTION NEURONS; PYRAMIDAL NEURONS; LAYER; SYNAPSES; ORGANIZATION; PLASTICITY; INPUTS;
D O I
10.1523/JNEUROSCI.2871-20.2023
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Activation of the primary motor cortex (M1) is important for the execution of skilled movements and motor learning, and its dysfunction contributes to the pathophysiology of Parkinson's disease (PD). A well-accepted idea in PD research, albeit not tested experimentally, is that the loss of midbrain dopamine leads to decreased activation of M1 by the motor thalamus. Here, we report that midbrain dopamine loss altered motor thalamus input in a laminar- and cell type-specific fashion and induced laminar-specific changes in intracortical synaptic transmission. Frequency-dependent changes in synaptic dynamics were also observed. Our results demonstrate that loss of midbrain dopaminergic neurons alters thalamocortical activation of M1 in both male and female mice, and provide novel insights into circuit mechanisms for motor cortex dysfunction in a mouse model of PD.
引用
收藏
页码:6021 / 6034
页数:14
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