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Fig. 6 | Journal of Neurodevelopmental Disorders

Fig. 6

From: Acamprosate in a mouse model of fragile X syndrome: modulation of spontaneous cortical activity, ERK1/2 activation, locomotor behavior, and anxiety

Fig. 6

Elevated zero maze (EZM). Wild-type and Fmr1 KO littermates were treated chronically with either saline or 122.2 mg/kg CaCl2 in saline (_Controls; equivalent amount of Ca2+ ions as in the 300 mg/kg acamprosate-treated group) or 300 mg/kg acamprosate in saline (+Acamp). The two control groups within each genotype were combined since no main effects of ‘control’ drug or ‘control’ drug interactions were found for any measures in the EZM during initial analysis, which included only saline and CaCl2-treated mice from each genotype. Control and Acamp-treated groups were analyzed by two-way ANOVA with pairwise comparisons corrected using FDR (two-tailed) when warranted. There was a significant main effect of gene and drug for time in open (a). Pairwise comparisons indicated a baseline genotype increase in time in open in the KO_Controls compared to the WT_Controls. Acamprosate treatment in the KO mice (KO + Acamp) further increased time in open compared to all other groups. No main effects or interactions were noted for Latency to first open arm entry (b). There was a significant main effect of gene for head dips (c) and transitions (d). Both KO groups had more head dips than the WT_Controls group. The KO + Acamp group had more open arm entries than the WT_Controls group. WT_Controls (n = 22), WT + Acamp (n = 11), KO_Controls (n = 20), KO + Acamp (n = 11); Data shown are LS mean ± SEM; *p < 0.05 for pairwise comparisons, N.S. = not significant

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