A delicate balance of neural activity is required during critical period in establishing innate odor preference.

The critical period in the mouse olfactory system is defined by activity-dependent synapse formation induced by Semaphorin7A/PlexinC1 signaling in the neonatal glomeruli.

Neurodevelopmental critical periods act to integrate activity to encode homeostatic set points that remain fixed thereafter.

Behavioral pharmacology and molecular biology reveal a translational control mechanism underlying auditory imprinting and structural plasticity that can be pharmacologically manipulated to reopen the critical period.

Neuromodulation of the expression of Hebbian plasticity enables rapid cortical sensory-induced remodeling in post-critical period adults, and can rescue deficits induced by prolonged sensory deprivation.

Visual impairment caused by monocular deprivation early in life can be reversed rapidly at older ages by temporarily blocking all activity in the non-deprived eye.

Sensory acquisition of a motor target is associated with rapid removal of excitatory synapses and with rapid insertion of inhibitory synapses in the main song control area of songbirds.

Sleep and wake states are not sufficient to drive changes in neocortical synaptic strengths.

Sensory deprivation suppresses cortical responsiveness through a selective remodeling of excitatory and inhibitory microcircuit motifs, by simultaneously amplifying feedforward and suppressing feedback excitation.

Adult neurogenesis in the olfactory bulb is not a turnover system but represents a lifelong neuronal addition mechanism.