Fig. 4

Aβ-mediated over-scaling in vivo requires CP-AMPARs. a1 Bilateral VD was performed in one month-old mice by sealing the eyelids with black epoxy and the animals were then kept in the dark. Prior to VD, Aβ (10 μg) or vehicle (water) was injected into V1 visual cortex via a cannula. Following 24 h VD, brain slices of the visual cortex were prepared for mEPSC recordings to examine synaptic scaling. a2 Sample mEPSC traces from brain slice recordings after the treatments shown to A1. a3 Quantification of the data shown in A2 (Control no VD = 12.2 ± 0.23, n = 7; Aβ no VD = 10.2 ± 0.48, n =6; Control after VD = 14.5 ± 0..19, n = 6; Aβ after VD = 16.6 ± 0.63, n = 6; 4 mice per condition). b1 Following 24 h VD paradigm, mEPSCs were recorded from brain slices with, or without PhTx, to determine the contribution of CP-AMPARs to HSP in vivo. b2 Sample mEPSC traces from brain slice recordings after the treatments shown to B1. b3 Quantification of the data shown in B2 (Control no VD + PhTx = 11.5 ± 0.33, n = 5; Aβ no VD + PhTx = 7.68 ± 0.21, n = 5; Control after VD + PhTx = 10.9 ± 0.21, n = 6; Aβ after VD + PhTx = 8.2 ± 0.63, n = 5; 4 mice per condition). Mann–Whitney U test, * p < 0.05, ** p < 0.01, *** p < 0.001, ns = not significant