Format

Send to

Choose Destination
BMB Rep. 2018 Jan;51(1):3-4.

Rebound excitability mediates motor abnormalities in Parkinson's disease.

Author information

1
Department of Biological Sciences, KAIST, Daejeon 34141, Korea; Center for Neuroscience, KIST, Seoul 02792, Korea.
2
Department of Biological Sciences, KAIST, Daejeon 34141, Korea.

Abstract

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. [BMB Reports 2018; 51(1): 3-4].

PMID:
29335072
PMCID:
PMC5796627
DOI:
10.5483/bmbrep.2018.51.1.004
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Korean Society for Biochemistry and Molecular Biology Icon for PubMed Central
Loading ...
Support Center