Cognitive dysfunction and bumetanide treatment in a valproate-induced rat model of autism

Cognitive dysfunction is an important aspect of the clinical characteristics of autism; however, research has often focused on social cognition. Learning and memory disorders often occur in autistic children, which are particularly under examined. Using cognitive and behavioral measures in our study, these disorders were endorsed in a valproate-induced rat model of autism. We identified increased levels of serum 5-hydroxytryptamine (5-HT) and gamma-aminobutyric acid (GABA), clear neuropathological changes, and enhanced protein expression levels of the N-methyl-D-aspartate (NMDA) receptor subunits NR2A and NR2B (NR2A, NR2B) and calcium/calmodulin-dependent protein kinase II (CaMK II), which suggests that these changes may have a role in the cognitive dysfunction of autism. Bumetanide has increasingly been used for the experimental treatment of autism. Thus, we treated model rats with Bumetanide and identified improvements in cognitive and behavioral measures. The current findings suggest that bumetanide may have potential long-term effects in the treatment of autism. Moreover, the effects of this drug may have a functional role through inhibition of the NKCC1 transporter.