Lili Guo1,2,5, Huan Xiong1,2,5, Jae-Ick Kim3.5, Yu-Wei Wu3.5, Rupa R Lalchandani3,4, Yuting Cui1,2, Yu Shu1,2, Tonghui Xu1,2 & Jun B Ding3,4
1Britton Chance Center for Biomedical Photonics, Wuhan National Laboratory for Optoelectronics.Huazhong University of Science and Technology, Wuhan, China. 2Ministry of Education (MoE) Key Laboratory for Biomedical Photonics, Department of Biomedical Engineering, Huazhong University of Science and Technology, Wuhan, China. 3Department of Neurosurgery, Stanford University School of Medicine, Palo Alto, California, USA. 4Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Palo Alto, California, USA. 5These authors contributed equally to this work.
Correspondence to : Tonghui Xu or Jun B Ding
Abstract
Dynamic adaptations in synaptic plasticity are critical for learning new motor skills and maintaining memory throughout life, which rapidly decline with Parkinson's disease (PD). Plasticity in the motor cortex is important for acquisition and maintenance of motor skills, but how the loss of dopamine in PD leads to disrupted structural and functional plasticity in the motor cortex is not well understood. Here we used mouse models of PD and two-photon imaging to show that dopamine depletion resulted in structural changes in the motor cortex. We further discovered that dopamine D1 and D2 receptor signaling selectively and distinctly regulated these aberrant changes in structural and functional plasticity. Our findings suggest that both D1 and D2 receptor signaling regulate motor cortex plasticity, and loss of dopamine results in atypical synaptic adaptations that may contribute to the impairment of motor performance and motor memory observed in PD.