Fig. 3.

RCAN1.1S overexpression leads to age-dependent impairments in synaptic plasticity. a One train of HFS (100 Hz) evoked similar levels of E-LTP in hippocampal area CA1 of young and aged TG mice compared to WT littermates (young F_(1,16) = .233, p = .636; aged F_(1,37) = .899, p = .349). n = 8–20 slices/group, 5–7 mice/group. b Four trains of HFS evoked similar L-LTP levels between young WT and TG mice (F_(1,14) = .067, p = .799). n = 7–9 slices/group, 5–7 mice/group. c L-LTP was significantly impaired in aged TG mice compared with WT littermates (F_(1,30) = .612, p = .019). n = 14–18 slices/group, 5–7 mice/group. Representative fEPSP recordings before (1 gray trace) and after LTP induction (2 black trace) at the top in a–c. d Western blot analysis of candidate RCAN1-regulated proteins important for synaptic plasticity in the aged mouse hippocampus. Impaired L-LTP in aged TG mice was not due to altered levels of phosphorylated GluA1 (p-GluA1) at S845 (t₍₁₉₎ = .037, p = .971) or S831 (t₍₁₉₎ = −.722, p = .479); total GluA1 (t₍₁₉₎ = .374, p = .713); NR2B phosphorylated at Y1472 (p-NR2B t₍₁₂₎ = .703, p = .495); total NR2B (t₍₁₂₎ = .832, p = .422); PSD95 (t₍₁₂₎ = 1.889, p = .083); synaptophysin (t₍₁₂₎ = .011, p = .991); CaMKII phosphorylated at T286 (p-CaMKII t₍₁₉₎ = .001, p = 1.00); or phosphorylated ERK at T202/Y204 (p-ERK1 t₍₁₉₎ = .143, p = .888; p-ERK2 t₍₁₉₎ = −.322, p = .751) in the hippocampus of aged TG mice compared to WT littermates. Phosphorylation signals normalized to the respective total protein levels; GluA1, NR2B, PSD95, and synaptophysin normalized to GAPDH. N = 6–12 mice/group. *p < .05