RESUMEN

Being a "behavioral disorder," autism spectrum disorder (ASD) is difficult to manage because its precise etiology is uncertain. In order to better understand the pathophysiology of autism and explore various therapeutic approaches, animal models are developed. Animal models of autism caused by valproate during pregnancy exhibit strong construct validity and reliability. Hence, this study was done among autism-induced rats with the aim of identifying the behavioral and biochemical assays. Pregnant rats were administered sodium valproate on the 12th day of gestation, while control pregnant rats received normal saline. The rats' offspring that received normal saline during intrauterine life were grouped as control, and the rats' offspring that received valproate were grouped as autism-induced. From postnatal day (PND) 21, behavioral assessments were done by using the Y maze (repetitive behavior) and the T maze (social behavior). The estimation of antioxidant profile (malondialdehyde {MDA}, glutathione {GSH}, catalase (CAT), and superoxide dismutase {SOD}), proinflammatory markers (tumor necrosis factor {TNF} alpha, transforming growth factor {TGF} beta, interleukin {IL} 6, and IL-1 beta), neurotransmitters (gamma-aminobutyric acid {GABA} and serotonin), and brain-derived neurotrophic factor (BDNF) in the hippocampal region was done. Oxidative stress, increased proinflammatory markers, and increased serotonin were recorded in the autism group. Rats with autism had a significant decrease in GABA and BDNF levels. These biochemical alterations can be correlated with clinical features of autism to diagnose and manage the disorder at the earliest.