Abstract
Autism spectrum disorder (ASD) is characterized by impaired social communication and repetitive/stereotyped behaviors. The neuropeptide oxytocin (OXT) plays a critical role in regulating social behaviors in the central nervous system, as indicated in both human and animal studies. We hypothesized that central OXT deficit is one of causes of etiology of ASD, which may be responsible for the social impairments. To test our hypothesis, central OXT system was examined in valproic acid (VPA)-induced rat model of autism (VPA rat). Our results showed that adolescent VPA rats exhibited a lower level of OXT mRNA and fewer OXT-ir cells in the hypothalamus than control rats. Additionally, OXT concentration in cerebrospinal fluid (CSF) was reduced. The number of OXT-ir cells in the supraoptic nucleus (SON) of neonatal VPA rats was also lower. Autistic-like behaviors were observed in these animals as well. We found that an acute intranasal administration of exogenous OXT restored the social preference of adolescent VPA rats. Additionally, early postnatal OXT treatment had long-term effects ameliorating the social impairments and repetitive behaviors of VPA rats until adolescence. This was accompanied by an increase in OXT-ir cells. Taken together, we demonstrated there was central OXT deficiency in the VPA-induced rat model of autism, and showed evidence that early postnatal OXT treatment had a long-term therapeutic effect on the autistic-like behaviors in VPA rats.
Highlights
Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder characterized by impaired social interaction and communication, as well as repetitive and stereotyped behavior (Bhat et al, 2014)
Results of isolation-induced Ultrasonic Vocalizations (USVs) test showed that the valproic acid (VPA) group emitted fewer USVs than the control group
Because of the close relationship between OXT and social behavior, we examined the role of OXT in the VPA-induced rat model of autism
Summary
Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder characterized by impaired social interaction and communication, as well as repetitive and stereotyped behavior (Bhat et al, 2014). Genetic factors are strongly indicated to be involved in the onset of ASD (Sebat et al, 2007; Klei et al, 2012; De Rubeis et al, 2014), they are not responsible for all cases. The etiology of ASD is believed to be a result of interactions between genetic and environmental factors (Hallmayer et al, 2011; Chaste and Leboyer, 2012; Tordjman et al, 2014). Specific medication for the treatment of the social impairments or language obstacles in ASD was lacking (McCracken et al, 2002; Bowers et al, 2015). A better understanding of the underlying mechanisms of ASD is necessary and which might provide treatment strategies in drug development
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