Association of Altered V1-M2 Neuronal Activation with Balance and Coordination Deficits in a Corneal Alkali Burn Mouse Model of Visual Impairment.

Visual impairment frequently impairs balance and motor coordination, yet the underlying neural circuit mechanisms remain poorly understood and require further investigation. In this study, we established a mouse model of visual impairment to assess the effects of defective vision on balance and coordination and further elucidated the functional role of the V1-M2 neural circuit in this process. A mouse model of corneal alkali burn was generated. Corneal morphology was observed, visual function was detected, and balance as well as motor coordination were evaluated. Neuronal activation in the V1 and M2 brain regions was quantified via c-Fos immunostaining. Viral tracing was performed to map the V1-M2 neural pathway, and chemogenetic manipulation was applied to modulate the V1-M2 circuit. Mice subjected to corneal alkali burn exhibited abnormal corneal morphology and impaired visual function, accompanied by significant deficits in balance and motor coordination. The number of c-Fos+ neurons was markedly reduced in both the V1 and M2 regions. The direct V1-M2 neural circuit was anatomically verified. Chemogenetic activation of the V1-M2 circuit elevated c-Fos expression in M2 and rescued impaired motor performance. Visual impairment disrupts balance and motor coordination in mice. The V1 and M2 cortical areas mediate this behavioral dysfunction, likely due to attenuated activation of the V1-M2 neural circuit. These findings identify a promising neural circuit for dissecting the fundamental mechanisms underlying visuomotor integration.