Journal
HORMONES AND BEHAVIOR
Volume 96, Issue -, Pages 130-136Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.yhbeh.2017.09.013
Keywords
Autism mouse model; Valproic acid; Oxytocin; Social interaction; Recognition memory
Categories
Funding
- JSPS KAKENHI [JP13J05359, JP25460099, JP16K08268, JP26293020, JP26670122, JP15H01288, 17H03989, JP16K15126]
- Neuropsychiatry Drug Discovery Consortium
- Osaka University
- Dainippon Sumitomo Pharma Joint Research Fund
- Uehara Memorial Foundation (Japan)
- Research Foundation for Pharmaceutical Sciences (Japan)
- JSPS Program for Advancing Strategic International Networks to Accelerate the Circulation of Talented Researchers [S2603]
- SRPBS from AMED
- Brain/MINDS from AMED
- Grants-in-Aid for Scientific Research [17H03989, 16K08268, 16K15126, 26293020] Funding Source: KAKEN
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Recent studies have reported that oxytocin ameliorates behavioral abnormalities in both animal models and individuals with autism spectrum disorders (ASD). However, the mechanisms underlying the ameliorating effects of oxytocin remain unclear. In this study, we examined the effects of intranasal oxytocin on impairments in social interaction and recognition memory in an ASD mouse model in which animals are prenatally exposed to valproic acid (VPA). We found that a single intranasal administration of oxytocin restored social interaction deficits for up to 2 h in mice prenatally exposed to VPA, but there was no effect on recognition memory impairments. Additionally, administration of oxytocin across 2 weeks improved prenatal VPA-induced social interaction deficits for at least 24 h. In contrast, there were no effects on the time spent sniffing in control mice. Immunohistochemical analysis revealed that intranasal administration of oxytocin increased c-Fos expression in the paraventricular nuclei (PVN), prefrontal cortex, and somatosensory cortex, but not the hippocampal CAI and CA3 regions of VPA-exposed mice, suggesting the former regions may underlie the effects of oxytocin. These findings suggest that oxytocin attenuates social interaction deficits through the activation of higher cortical areas and the PVN in an ASD mouse model.
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