Journal
JOURNAL OF NEUROCHEMISTRY
Volume 138, Issue 1, Pages 117-123Publisher
WILEY
DOI: 10.1111/jnc.13634
Keywords
HPC-1/syntaxin 1A; in vivo microdialysis; knockout mice; oxytocin; SNARE protein; social behavior
Categories
Funding
- Ministry of Education, Culture, Sports, Science and Technology, Japan [22500338, 24300142]
- Promotion and Mutual Aid Cooperation for Private Schools of Japan
- Grants-in-Aid for Scientific Research [22500338] Funding Source: KAKEN
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HPC-1/syntaxin1A (STX1A), a neuronal soluble N-ethylmaleimide-sensitive fusion attachment protein receptor, contributes to neural function in the CNS by regulating transmitter release. Recent studies reported that STX1A is associated with human neuropsychological disorders, such as autism spectrum disorder and attention deficit hyperactivity disorder. Previously, we showed that STX1A null mutant mice (STX1A KO) exhibit neuropsychological abnormalities, such as fear memory deficits, attenuation of latent inhibition, and unusual social behavior. These observations suggested that STX1A may be involved in the neuropsychological basis of these abnormalities. Here, to study the neural basis of social behavior, we analyzed the profile of unusual social behavior in STX1A KO with a social novelty preference test, which is a useful method for quantification of social behavior. Interestingly, the unusual social behavior in STX1A KO was partially rescued by intracerebroventricular administration of oxytocin (OXT). In vivo microdialysis studies revealed that the extracellular OXT concentration in the CNS of STX1A KO was significantly lower compared with wild- type mice. Furthermore, dopamine-induced OXT release was reduced in STX1A KO. These results suggested that STX1A plays an important role in social behavior through regulation of the OXTergic neural system.
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