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

Area of Science:

• Neuroscience
• Motor control
• Neural plasticity

Background:

• Cortical plasticity is crucial for motor recovery after brain injury.
• The functional circuit mechanisms underlying this plasticity remain unclear.

Purpose of the Study:

• To investigate motor recovery and neural plasticity following optogenetic suppression of a specific cortical area involved in eye movement.
• To elucidate the functional circuit-level changes that mediate recovery.

Main Methods:

• Optogenetic suppression of the secondary motor cortex (MOs) in mice performing a visually-guided eye movement task.
• Longitudinal two-photon calcium imaging to monitor neural activity.
• Behavioral assessment of eye movement control.

Main Results:

• Unilateral MOs suppression initially impaired contraversive eye movements.
• Over time, the suppression became less effective, and movement capability was restored.
• Regained movement capability correlated with increased ipsiversive movement encoding neurons in the contralateral MOs.
• Further suppression of the contralateral MOs disrupted the recovered movement, suggesting compensation.

Conclusions:

• Repeated optogenetic suppression induces functional recovery in motor control.
• This recovery is mediated by compensatory neural mechanisms in the contralateral hemisphere.
• The findings highlight the adaptive capacity of neural circuits following perturbation.