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In adult mice, monocular enucleation (ME) results in an immediate deactivation of the contralateral medial monocular visual cortex. An early restricted reactivation by open eye potentiation is followed by a late overt cross-modal reactivation by whiskers (Van Brussel et al., 2011). In adolescence (P45), extensive recovery of cortical activity after ME fails as a result of suppression or functional immaturity of the cross-modal mechanisms (Nys et al., 2014). Here, we show that dark exposure before ME in adulthood also prevents the late cross-modal reactivation component, thereby converting the outcome of long-term ME into a more P45-like response. Because dark exposure affects GABAergic synaptic transmission in binocular V1 and the plastic immunity observed at P45 is reminiscent of the refractory period for inhibitory plasticity reported by Huang et al. (2010), we molecularly examined whether GABAergic inhibition also regulates ME-induced cross-modal plasticity. Comparison of the adaptation of the medial monocular and binocular cortices to long-term ME or dark exposure or a combinatorial deprivation revealed striking differences. In the medial monocular cortex, cortical inhibition via the GABAA receptor α1 subunit restricts cross-modal plasticity in P45 mice but is relaxed in adults to allow the whisker-mediated reactivation. In line, in vivo pharmacological activation of α1 subunit-containing GABAA receptors in adult ME mice specifically reduces the cross-modal aspect of reactivation. Together with region-specific changes in glutamate acid decarboxylase (GAD) and vesicular GABA transporter expression, these findings put intracortical inhibition forward as an important regulator of the age-, experience-, and cortical region-dependent cross-modal response to unilateral visual deprivation.

Regional Specificity of GABAergic Regulation of Cross-Modal Plasticity in Mouse Visual Cortex after Unilateral Enucleation