Fig. 1

VPA reinstates ocular dominance plasticity in adult visual cortex. a The mouse visual system is naturally skewed toward the contralateral eye. Unlike during the CP [32], brief monocular deprivation (4d MD) fails to alter this ocular dominance of V1 neurons rated on a seven-point scale (white bars). b Upon VPA administration (6d) prior to and concurrent with adult MD, responsiveness once again can shift in favor of the open eye (black bars; n = 98 and 103 cells from n = 4 mice per group, CBI = 0.72 and 0.51, respectively; p < 0.001, χ ² test). c Significant CBI reduction by MD occurs only with VPA (closed circles, p = 0.0002, unpaired two tailed t test versus vehicle, open circles). Enhancing inhibition, an alternative consequence of VPA treatment [33], is insufficient to induce adult plasticity, as benzodiazepine agonists (DZ, closed triangles; Veh, open triangles) fail to reduce CBI. d Reduction of histone deacetylase (HDAC) activity within 2 h of either valproic acid (VPA) or trichostatin A (TSA) administration. HDAC activity normalized to vehicle (***p = 0.0004, **p = 0.0024; unpaired two-tailed t test, n = 3 per group). e Treatment with HDACi re-activates the critical period in adult mice