Visual deprivation reactivates rapid ocular dominance plasticity in adult visual cortex

Abstract

Brief monocular deprivation (< or =3 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 GABAA 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.

Figures

Figure 1.

Visual deprivation reactivates rapid, juvenile-like ocular dominance plasticity in the adult visual cortex. A, Brief (3 d) MD does not induce an ocular dominance shift in light-reared adults. Left, VEP amplitudes (C/I) recorded from each subject in the visual cortex ipsilateral and contralateral to the occluded eye. Right, Summary data reveal no significant difference in VEP C/I across two hemispheres. Inset, Representative VEPs (average of 100 trials) recorded from each hemisphere in response to stimulation of the occluded (filled circle) and open (open circle) eye. Calibration: 100 ms, 50 μV. B, Brief MD after 10 d of visual deprivation induces a significant ocular dominance shift. Left, VEP C/I from each subject. Right, Summary data reveals a significant difference in VEP C/I across two hemispheres, indicating an ocular dominance shift (**p < 0.01, paired t test). Inset, Representative VEPs (average of 100 trials). C, In visually deprived adults, brief MD induces a significant depression in the response to stimulation of the occluded eye and a significant potentiation in the response to stimulation of open eye in the visual cortex (VCtx) contralateral to the occlusion (**p < 0.01 vs light-reared controls, unpaired t test). No difference in the response to stimulation of either eye was observed in the visual cortex ipsilateral to the occlusion (p > 0.05, unpaired t test). amp, Amplitude. Error bars represent SEM.

Figure 2.

Visual deprivation induces persistent reactivation of rapid ocular dominance plasticity in adults. Adults received brief MD immediately after 10 d of visual deprivation or when 1, 3, or 7 d of binocular vision was allowed after visual deprivation. C/I VEPs reveal that brief MD continued to effectively induce an OD shift in the visual cortex (VCtx) contralateral to the occluded eye, when 1 or 3 d, but not 7 d, of binocular vision follows visual deprivation (**p < 0.01, one-way ANOVA with post hoc analysis). We see no difference in the C/I VEP in the visual cortex ipsilateral to the occluded eye. Error bars represent SEM.

Figure 3.

Visual deprivation in adults reverses two molecular correlates of cortical maturation. A, Top, Representative immunoblots for GABAAβ2/3 and GluR2 from juvenile and adult visual cortical homogenate. Bottom, Summary data demonstrate that visual deprivation induces a significant decrease in GABAAβ2/3 relative to GluR2 in juveniles and adults (*p < 0.05, unpaired t test). B, Top, Representative immunoblots for NR2b and NR2a from juvenile and adult visual cortical synaptoneurosomes. Bottom, Summary data demonstrate that visual deprivation induces a significant increase in NR2b relative to NR2a in juveniles and adults (*p < 0.01, unpaired t test). Data were normalized to age-matched LR for display. Error bars represent SEM.