Department of Neuroscience, Medical University of South Carolina, Charleston, United States; Center for Integrative Neuroscience, University of Tübingen, Tübingen, Germany; Department of Mental Disorder Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan; JST, PRESTO, Kawaguchi, Japan
Takahide Itokazu
Center for Integrative Neuroscience, University of Tübingen, Tübingen, Germany; Department of Neuro-Medical Science, Osaka University, Osaka, Japan
Center for Integrative Neuroscience, University of Tübingen, Tübingen, Germany; Department of Physiology, Tokyo Women’s Medical University, Tokyo, Japan
Makoto Ohtake
Department of Neuroscience, Medical University of South Carolina, Charleston, United States; Department of Neurosurgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan
Tetsuya Yamamoto
Department of Neurosurgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan
Kazuhiro Sohya
Department of Mental Disorder Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan
Takakuni Maki
Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan
JST, PRESTO, Kawaguchi, Japan; Department of Physiology, Monash University, Clayton, Australia; Neuroscience Program, Biomedicine Discovery Institute, Monash University, Clayton, Australia
Cortical plasticity is fundamental to motor recovery following cortical perturbation. However, it is still unclear how this plasticity is induced at a functional circuit level. Here, we investigated motor recovery and underlying neural plasticity upon optogenetic suppression of a cortical area for eye movement. Using a visually-guided eye movement task in mice, we suppressed a portion of the secondary motor cortex (MOs) that encodes contraversive eye movement. Optogenetic unilateral suppression severely impaired contraversive movement on the first day. However, on subsequent days the suppression became inefficient and capability for the movement was restored. Longitudinal two-photon calcium imaging revealed that the regained capability was accompanied by an increased number of neurons encoding for ipsiversive movement in the unsuppressed contralateral MOs. Additional suppression of the contralateral MOs impaired the recovered movement again, indicating a compensatory mechanism. Our findings demonstrate that repeated optogenetic suppression leads to functional recovery mediated by the contralateral hemisphere.
