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Although bumetanide,which is believed to improve the symptoms of autism,is widely used clinically,the research on its mechanism remains limited.Studies have also shown that cognitive impairment is closely linked to autism clinical characteristics.Using a valproate (VPA)-induced rat autism model,we observed morphological changes to the frontal lobe and hippocampus,detected the levels of 5-hydroxytryptamine (5-HT),gamma-amino acid butyric acid (GABA),and Glu in serum,and measured the expression of N-Methyl-D-aspartate (NMDA) receptor subunits NR2A and NR2B and calcium/calmodulin-dependent protein kinase II (CamK II) in the brain tissue.In addition,we used western blots to investigate the pathogenesis of cognitive impairment in autism and the mechanism underlying the effect of bumetanide.Autistic rats showed distinct nerve pathological changes,increased serum levels of 5-HT and GABA,and increased protein expression levels of NR2A,NR2B,and CamK II in the brain tissue,which likely contribute to autism behaviors and cognitive dysfunction.Bumetanide significantly improved autism behavior and cognitive dysfunction.The mechanism of bumetanide action may be through inhibition of the NKCC1 transporter,which can reduce the concentration of CI" in cells,and regulates the function of GABA.