Open AccessDyskinesia is Closely Associated with Synchronization of Theta Oscillatory Activity Between the Substantia Nigra Pars Reticulata and Motor Cortex in the Off L-dopa State in Rats
Author(s) -
Jiazhi Chen,
Qiang Wang,
Nanxiang Li,
Shujie Huang,
Min Li,
Jiyang Cai,
Yuzheng Wang,
Huantao Wen,
Siyuan Lv,
Ning Wang,
Jinyan Wang,
Fei Luo,
Wangming Zhang
Publication year - 2020
Publication title -
neuroscience bulletin/neuroscience bulletin
Language(s) - English
Resource type - Journals
eISSN - 1673-7067
pISSN - 1995-8218
DOI - 10.1007/s12264-020-00606-3
Subject(s) - dyskinesia , neuroscience , substantia nigra , parkinson's disease , basal ganglia , levodopa , psychology , motor cortex , cortex (anatomy) , premovement neuronal activity , inhibitory postsynaptic potential , medicine , dopamine , central nervous system , stimulation , disease , dopaminergic
Excessive theta (θ) frequency oscillation and synchronization in the basal ganglia (BG) has been reported in elderly parkinsonian patients and animal models of levodopa (L-dopa)-induced dyskinesia (LID), particularly the θ oscillation recorded during periods when L-dopa is withdrawn (the off L-dopa state). To gain insight into processes underlying this activity, we explored the relationship between primary motor cortex (M1) oscillatory activity and BG output in LID. We recorded local field potentials in the substantia nigra pars reticulata (SNr) and M1 of awake, inattentive resting rats before and after L-dopa priming in Sham control, Parkinson disease model, and LID model groups. We found that chronic L-dopa increased θ synchronization and information flow between the SNr and M1 in off L-dopa state LID rats, with a SNr-to-M1 flow directionality. Compared with the on state, θ oscillational activity (θ synchronization and information flow) during the off state were more closely associated with abnormal involuntary movements. Our findings indicate that θ oscillation in M1 may be consequent to abnormal synchronous discharges in the BG and support the notion that M1 θ oscillation may participate in the induction of dyskinesia.