Increased self-grooming gates adult visual cortical plasticity through a ventral pallidum-visual cortex pathway

Repetitive behaviors are prominent features of multiple neurodevelopmental and psychiatric disorders, which are frequently accompanied by abnormalities in visual processing. However, whether repetitive behavioral states themselves actively regulate visual system, and through what neural mechanisms, remains unclear. Using a water-spray paradigm that selectively increased self-grooming in male mice, we showed ocular-dominance plasticity in adult primary visual cortex (V1) was markedly enhanced. Neurons in the ventral pallidum (VP) were activated in synchrony with self-grooming behavior. VP inhibition abolished both grooming and plasticity, whereas VP activation was sufficient to boost both. Viral tracing identified a direct, predominantly GABAergic VP→V1 projection whose activity controlled V1 E/I balance and grooming-induced plasticity. In a pharmacological model of compulsive grooming induced by repeated meta-chlorophenylpiperazine (mCPP) administration, grooming intensity positively correlated with visual plasticity in a VP-dependent manner. Together, these findings identified the VP-V1 pathway as a critical circuit through which a grooming-associated behavioral state modulated adult visual cortical plasticity, revealing a previously unrecognized link between behavioral state and sensory cortical function. Significance Statement Repetitive behaviors are a hallmark of many neuropsychiatric disorders and are often accompanied by sensory abnormalities. This paper identifies a ventral pallidum to primary visual cortex circuit that links self-grooming-associated state to the modulation of visual cortical plasticity in adult mice. These findings may provide a potential mechanism through which repetitive behaviors may directly influence sensory cortical function and contribute to maladaptive sensory reorganization in neuropsychiatric disorders.