Conclusion
Our results show that ceftriaxone did not exert significant therapeutic effect on VPA-induced mouse model of autism.
Methods
A total of 96 BALB/c male mice were divided into 12 groups (n = 8 animals per group). Ceftriaxone (50, 100, 200 mg/kg/d) or saline was given to the male offsprings born from pregnant mice administered VPA and/or saline, between days 47 and 55. Dihydrokainic acid (10 mg/kg), a GLT-1 inhibitor, was administered intraperitoneally to evaluate whether GLT-1 mediates the effect of ceftriaxone. Three chamber sociability and social interaction test and the rota rod test were performed in all groups on days 54 and 55. GLT-1 levels in the hippocampus were measured by immunohistochemistry (IHC) and western blotting (WB).
Purpose
Autism is a multifactorial neurodevelopment disease and it has not been disclosed as a hypoglutamatergic or hyperglutamathergic disease. Ceftriaxone is an antibiotic that increases glutamate transporter-1 (GLT-1) expression in the brain in chronic use. In our study we aimed to investigate the effects of different doses of ceftriaxone in postnatal period in male mice exposed to valproic acid (VPA) at 12.5th day of pregnancy.
Results
In our study, autism-like behaviors were observed in male offsprings that were exposed to VPA in the intrauterine period. Chronic ceftriaxone administration has no curative effect on behavioral impairment seen in autism.