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.
Highlights
Neural plasticity in motor cortex is critical for motor learning (Peters et al, 2017), and for motor recovery following cortical damage (Nudo, 2013)
To establish a circuit basis of the neural plasticity underlying motor recovery, we investigated the neural representation of eye movements during a visually-guided eye movement task that we previously developed (Itokazu et al, 2018)
We investigated the contribution of the contralateral hemisphere to eye movement recovery following suppression of the unilateral motor cortex
Summary
Neural plasticity in motor cortex is critical for motor learning (Peters et al, 2017), and for motor recovery following cortical damage (Nudo, 2013). Previous studies in rodents investigated the cellular and molecular mechanisms that underlie compensatory pathophysiological changes in the cortical network during stroke recovery (Alia et al, 2017; Fawcett, 2015; Li et al, 2010; Schwab and Strittmatter, 2014) Such changes include modification of extracellular matrix structures (Fawcett, 2015) and increased neurotropic factors for angiogenesis, neurogenesis, and synaptic plasticity. Like binocularly coupled saccade, shows a simple but robust motor output, and its direction is represented mainly in the contralateral frontal cortex Consistent with this representation, a unilateral lesion in primate frontal cortex disrupts saccades toward the contralateral side (i.e., contraversive saccades) (Crowne et al, 1981; Pierrot-Deseilligny et al, 2002; van der Steen et al, 1986). Such plasticity could represent the neural basis of motor recovery
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