Rebound excitability mediates motor abnormalities in Parkinson's disease

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Parkinson's disease (PD) is a debilitating disorder resulting from loss of dopamine neurons. In dopamine deficient state, the basal ganglia increases inhibitory synaptic outputs to the thalamus. This increased inhibition by the basal ganglia output is known to reduce firing rate of thalamic neurons that relay motor signals to the motor cortex. This 'rate model' suggests that the reduced excitability of thalamic neurons is the key for inducing motor abnormalities in PD patients. We reveal that in response to inhibition, thalamic neurons generate rebound firing at the end of inhibition. This rebound firing increases motor cortical activity and induces muscular responses that triggers Parkinsonian motor dysfunction. Genetic and optogenetic intervention of the rebound firing prevent motor dysfunction in a mouse model of PD. Our results suggest that inhibitory synaptic mechanism mediates motor dysfunction by generating rebound excitability in the thalamocortical pathway.
Publisher
KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
Issue Date
2018-01
Language
English
Article Type
Editorial Material
Citation

BMB REPORTS, v.51, no.1, pp.3 - 4

ISSN
1976-6696
DOI
10.5483/BMBRep.2018.51.1.004
URI
http://hdl.handle.net/10203/240394
Appears in Collection
BS-Journal Papers(저널논문)
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