Journal: Molecular Medicine Reports
Article Title: The GABAB receptor agonist STX209 reverses the autism-like behaviour in an animal model of autism induced by prenatal exposure to valproic acid
doi: 10.3892/mmr.2022.12670
Figure Lengend Snippet: Prenatal VPA exposure causes GABAergic system function defects in the hippocampus of VPA model mice, and nervous system damage in the CA1 and DG regions of the hippocampus in the mice. STX209 ameliorates these defects. Representative western blotting images showing the expression levels of (A) GABABR2 and (B) GAD65/67 protein in the entire hippocampus in each group. Histograms of the relative expression levels of (C) GABABR2 and (D) GAD65/67 proteins in each group (n=3 mice from different mothers/group; western blotting was repeated once). Chronic administration of STX209 did not increase GAD65/67 expression in VPA model mice but elevated the expression level of GABABR2. **P<0.01, ***P<0.001 (two-way ANOVA followed by Bonferroni post hoc test). All data are presented as the mean ± SEM. CTRL, control; NS, normal saline; GABABR2, γ-aminobutyric acid type B receptor 2; GAD65/67, glutamic acid decarboxylase 65/67; VPA, valproic acid; ns, no significance.
Article Snippet: STX209 (MedChemExpress) was administered intraperitoneally to CTRL+STX20 and VPA+STX209 group mice at a dose of 0.6 mg/kg in 0.9% NS twice a day from weaning (P21) until the end of the experiment (approximately P60) ( ).
Techniques: Western Blot, Expressing, Saline