Neural circuits are shaped by experience - the potency of which changes dynamically across the lifespan. Two important concepts have emerged from the study of such 'critical periods': 1) excitatory-inhibitory circuit balance is a trigger; and 2) molecular 'brakes' limit adult plasticity. Thus, the critical period per se is plastic, and one outcome of normal development is then to stabilize the neural networks initially sculpted by experience. This talk focuses on fast-spiking parvalbumin circuits in particular, as they are pivotal hubs for plasticity and consistently vulnerable in neurological disorders. Genetic or pharmacological manipulations are so powerful that animals of identical chronological age may be at the peak, before, or past their plastic window. Notably, the cellular and molecular factors which control onset and closure of plasticity are often linked to genes implicated in mental illness, suggesting mis-regulated developmental trajectories as part of the etiology. The emerging notion that the brain's intrinsic potential for plasticity may be actively dampened (rather than passively lost), the associated biological cost of maintaining multiple brakes throughout life, why there are so many, how they interact and ultimately how to lift them in non-invasive ways may hold the key to correcting devastating neurodevelopmental disorders, recovery from brain injury in adulthood and sustaining life-long learning more broadly.