New Treatment Helps Prevent Autistic Behavior in Rodents

In neonatal mammals, γ-aminobutyric acid (GABA) switches from being an excitatory neurotransmitter to being an inhibitory neurotransmitter. The surge of maternal oxytocin at birth affects chloride channels in fetal neurons, causing chloride concentrations to drop — and the “GABA switch” to be activated. In contrast, in two rodent models of autism, chloride concentrations remain high and GABA remains an excitatory neurotransmitter after birth.

Using rats from these autism models, a French team administered an FDA-approved diuretic, bumetanide, to rodent mothers 1 day before delivery. The treatment triggered the change in chloride concentrations, activated the GABA switch, and eliminated autistic behavior in offspring.