Interhemispherically dynamic representation of an eye movement-related activity in mouse frontal cortex

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Abstract

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.

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The source data are included in the manuscript and supporting files.

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Takashi R Sato

Department of Neuroscience, Medical University of South Carolina, Charleston, United States

For correspondence
satot@musc.edu

Competing interests
The authors declare that no competing interests exist.

"This ORCID iD identifies the author of this article:" 0000-0002-7623-9021
Takahide Itokazu

Department of Neuro-Medical Science, Osaka University, Suita, Japan

Competing interests
The authors declare that no competing interests exist.
Hironobu Osaki

Department of Physiology, Tokyo Women's Medical University, Tokyo, Japan

Competing interests
The authors declare that no competing interests exist.

"This ORCID iD identifies the author of this article:" 0000-0001-9780-0810
Makoto Ohtake

Department of Neuroscience, Medical University of South Carolina, Charleston, United States

Competing interests
The authors declare that no competing interests exist.
Tetsuya Yamamoto

Department of Neurosurgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan

Competing interests
The authors declare that no competing interests exist.
Kazuhiro Sohya

Department of Mental Disorder Research, National Center of Neurology and Psychiatry, Tokyo, Japan

Competing interests
The authors declare that no competing interests exist.
Takakuni Maki

Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan

Competing interests
The authors declare that no competing interests exist.
Tatsuo K Sato

Department of Physiology, Biomedicine Discovery Institute, Monash University, Clayton, Australia

For correspondence
tatsuo.sato@monash.edu

Competing interests
The authors declare that no competing interests exist.

Funding

Japan Science and Technology Agency (PRESTO)

Takashi R Sato

Deutsche Forschungsgemeinschaft (SA 2575/2-1)

Takashi R Sato

Japan Science and Technology Agency (PRESTO)

Tatsuo K Sato

Deutsche Forschungsgemeinschaft (SA 2575/3-1)

Takashi R Sato

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Ethics

Animal experimentation: All experimental procedures were approved by the University of Tuebingen (IN4/11) Medical University of South Carolina (IACUC-2018-00352), and National Center of Neurology and Psychiatry (2014005).

Copyright

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.