Figure 7
From: Chondroitin Sulfate Is Required for Onset and Offset of Critical Period Plasticity in Visual Cortex
The offset of visual plasticity is also prevented in both T1 and Otx2 KO mice. (A) Prolonged neuronal firing is elevated in T1 KO mice (KO + Veh) and reduced by DZ treatment (KO + DZ) as well as WT mice (10–16 mice, WT 1.8 ± 1.0 versus vehicle-injected KO 16.7 ± 3.7, p < 0.0001, DZ-injected KO 2.4 ± 0.8 versus vehicle-injected KO, p < 0.0001, ANOVA). Error bar represents SEM. (B) CBI values of vehicle-injected T1 KO mice are typically high with MD over P60 (KO + Veh, 0.70 ± 0.01). Reduction in CBI values is induced in DZ-treated KO with MD over P60 (+DZ, 0.59 ± 0.01, versus + Veh, p < 0.0001, t-test) as well as at P24 (+DZ, 0.59 ± 0.002). (C) High CBI values in the deprived control (Cont, 0.69 ± 0.01) and Otx2 KO mice (KO + Veh, 0.67 ± 0.01; open symbols, non-injected; gray symbols, vehicle-injected) are significantly reduced by DZ injection (+DZ, 0.59 ± 0.02) even in the adult (>P60) (KO + Veh versus + DZ, p = 0.0003, t-test). (D) Prolonged critical period in T1 KO mice. Ocular dominance shift following MD (toward group 4) is observed even 1 month later after DZ at P24 (T1 KO + DZ), but not after vehicle injection (T1 KO + Veh) (p < 0.0001, χ2-test). (E) High CBI values in deprived T1 KO (0.69 ± 0.01) or Otx2 KO mice (0.70 ± 0.01, Veh, vehicle-injected mice) are reduced long after the onset in DZ-injected mice (DZ, T1 KO, 0.58 ± 0.01 versus Veh, p < 0.0001; Otx2 KO, 0.58 ± 0.01 versus Veh, p = 0.0003, t-test). (F) Otx2 removal by cortical infusion of an inhibitory antibody (α-Otx2) reactivates plasticity in adult WT mice (WT + Veh, vehicle-infused; WT + α-Otx2, antibody-infused; p < 0.0001, χ2-test). (G) Ocular dominance shift (low CBI) in individual mice is induced by acute inhibitory antibody (α-Otx2) with MD (Veh, 0.70 ± 0.02 versus α-Otx2, 0.59 ± 0.01, p = 0.004, t-test).
