Brief monocular deprivation (Յ3 d) induces a rapid shift in the ocular dominance of binocular neurons in the juvenile rodent visual cortex but is ineffective in adults. Here, we report that persistent, rapid, juvenile-like ocular dominance plasticity can be reactivated in adult rodent visual cortex when monocular deprivation is preceded by visual deprivation. Ocular dominance shifts in visually deprived adults are caused by a rapid depression of the response to stimulation of the deprived eye, previously only reported in juveniles, and a simultaneous potentiation of the response to stimulation of the nondeprived eye. The enhanced ocular dominance plasticity induced by visual deprivation persists for days, even if binocular vision precedes monocular deprivation. Visual deprivation also induces a significant decrease in the level of GABA A receptors relative to AMPA receptors and a return to the juvenile form of NMDA receptors in the visual cortex, two molecular changes that we propose enable the persistent reactivation of rapid ocular dominance plasticity.
The shift in ocular dominance induced by brief monocular deprivation is greatest during a postnatal critical period and is thought to decline irreversibly thereafter. However, here we demonstrate that complete visual deprivation through dark exposure restores rapid ocular dominance plasticity in adult rats. In addition, the loss of visual acuity resulting from chronic monocular deprivation is reversed if dark exposure precedes removal of the occlusion in adulthood, suggesting a potential use for dark exposure in the treatment of adult amblyopia.
Restricted receptive fields (RFs), a hallmark of mature sensory systems, are actively maintained by a balance between ascending excitation and local inhibition in the cortex. Deafferentation disrupts this balance, allowing a sequence of changes in neuronal response properties that culminate in the reorganization of cortical RFs. To explore the molecular basis of deafferentation-induced RF reorganization, we tracked changes in AMPA receptor (AMPAR), NMDA receptor (NMDAR) and GABA A receptor (GABA A R) levels in the deafferented somatosensory cortex of adult raccoons following single-digit amputation. In synaptoneurosomes prepared from deafferented cortex, we observe a significant increase in AMPARs, but no change in NMDARs, 1-9 days post-deafferentation, coincident with the appearance of new excitatory inputs and enlarged RFs. We observe a significant increase in GABA A Rs 2-7 weeks post-deafferentation, coincident with a return of inhibitory input and shrinking RFs. These experiencedependent changes in the levels of the major cortical ionotropic receptors were transient, returning to pre-experimental baseline by ‡ 17 weeks post-deafferentation, when RFs return to original size, but are remapped to different loci. This suggests that deafferentation-induced cortical reorganization may be generated by activity-dependent potentiation of weak excitatory synapses, followed by an increase in the strength of inhibitory synapses, resulting in finely tuned, remapped cortical RFs.
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