The bursts bear resemblance to in vivo gamma-oscillatory activity found in rat ASD models with respect to their gamma frequency spectrum, their origin (in the CA1), and their sensitivity to blockers of cation-chloride pumps (NKCC1 and KCC2), as well as to oxytocin.
Reduced KCC2 levels in the neuronal membrane contribute to the generation of epilepsy, neuropathic pain, and autism spectrum disorders; thus, it is important to characterize the mechanisms regulating KCC2 expression.
These results suggest alterations in m-GABA<sub>A</sub>Rβ3 levels, KCC2 levels, and trafficking of GABA<sub>A</sub>Rs in rats prenatally exposed to valproic acid and advance our understanding of the pathogenesis of ASD.