Our behavior reflects the neural circuits sculpted by our experiences during early temporary windows of heightened brain plasticity called critical periods. Such heightened plasticity declines in adulthood, often limiting recovery of function. On the other hand, the adult brain also needs stability. Failed stabilization can disrupt circuit computations by allowing modification by undesirable information, which may lead to mental disorders. Understanding the mechanisms regulating the critical periods of neural plasticity can provide insights toward therapeutic interventions for neurodevelopmental and psychiatric disorders. In this review, we discuss the potential contributions of "molecular brakes" on the critical period plasticity in the visual system to the etiology of psychiatric disorders. Interestingly, recent findings for the pathophysiological changes associated with schizophrenia indicate excessive plasticity due to the removal of molecular brakes. Applying the mechanistic understandings of critical period plasticity in the visual system to cognitive development may provide a conceptual framework for exploring novel endophenotypes and therapeutic approaches to treat psychiatric disorders.