Bright-light treatment ameliorates motor and non-motor deficits through distinct visual circuits in a mouse model of Parkinson's disease.

Light has a profound impact on non-visual functions, and clinical evidence suggests bright-light therapy's effectiveness in alleviating motor and non-motor symptoms of Parkinson's disease (PD). However, the neural mechanisms underlying these effects remain unclear. Here, we demonstrate that bright-light treatment alleviates PD symptoms in mice via distinct visual circuits. Specifically, bright-light signals transmitted by the ventral lateral geniculate nucleus alleviate non-motor symptoms, such as depressive-like behaviors and spatial memory deficits. Conversely, the improvement in motor symptoms with bright-light treatment depends on a separate, disynaptic visual pathway that connects the superficial layers of the superior colliculus to the substantia nigra pars compacta (SNc). Notably, in this pathway, bright-light signals enhance the bursting activity of SNc dopaminergic neurons by upregulating HCN2 expression, a mechanism essential for motor improvements. These findings provide valuable insights into the neural mechanisms by which bright-light therapy benefits PD.