A Mouse Model of the Human Fragile X Syndrome I304N Mutation
Figure 3
Protein synthesis-independent mGluR-LTD in Fmr1I304N mice.
Evoked extracellular field potentials (FPs) from CA1 of acute slices from 30–90 day old wild-type and B6.Fmr1I304N littermates are plotted as a percent of baseline (pre-DHPG or PP-LFS). (A,B) Anisomycin inhibits DHPG-induced LTD in wild-type littermates, but has no effect in B6.Fmr1I304N mice (*; p = 0.02). (C,D) Anisomycin inhibits synaptically induced LTD (with PP-LFS; *; p = 0.004) in wild type mice, but not B6.Fmr1I304N mice. The magnitude of LTD between wild type and Fmr1I304N mice is not different under control conditions, but is enhanced in the presence of anisomycin (ANOVA and subsequent Fisher PLSD; p<0.05). (E) There is no difference in the degree of LTD elicited by DHPG stimulation between B6.Fmr1I304N mice and their Fmr1 null littermates.