Molecular strategies for recovery from amblyopia

Recovery from amblyopia, an enduring loss of vision caused by abnormal visual experience early in life, is generally limited in adulthood across species from human to rodents. Recent research in rodents identified novel strategies for functional recovery. We recently identified an increase in expression of the Lynx1 protein in mice that prevented plasticity in the primary visual cortex late in life. Removal of this molecular brake enhanced nicotinic acetylcholine receptor signaling. Lynx1 expression thus maintains stability of mature cortical networks in the presence of cholinergic innervation. Resetting an excitatory-inhibitory balance or removing molecular 'brakes' on structural plasticity may unmask the potential for recovery of function in adulthood. Novel pharmacological or environmental interventions now hold great therapeutic promise based on a deeper understanding of critical period mechanisms.