Kim, Jeongjin Kim, Daesoo 2024-01-19T23:34:24Z 2024-01-19T23:34:24Z 2021-09-03 2018-01 1976-6696 https://pubs.kist.re.kr/handle/201004/121875 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. English KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY Rebound excitability mediates motor abnormalities in Parkinson's disease Article 10.5483/BMBRep.2018.51.1.004 1 BMB REPORTS, v.51, no.1, pp.3 - 4 BMB REPORTS 51 1 3 4 scie scopus kci 000424213100002 2-s2.0-85042005437 Biochemistry & Molecular Biology Biochemistry & Molecular Biology Editorial Material Basal ganglia Parkinson&apos s disease Rebound firing Thalamus T-type Ca2+ channels