Kamikihito ameliorates social recognition in oxytocin gene deficient mice and environmentally induced autism spectrum disorder model mice.

Researchers tested a traditional Japanese herbal medicine called Kamikihito on mice with autism-like social difficulties. The treatment helped improve social recognition in some mouse models, particularly those missing the hormone oxytocin. The medicine seemed to work by calming overactive brain responses during social situations. While promising, this is early research in animals only.

This preclinical study investigated Kamikihito (KKT), a traditional Japanese medicine, as a potential treatment for social recognition deficits characteristic of autism spectrum disorder. Using multiple mouse models including oxytocin knockout mice and LPS-induced ASD models, researchers found that KKT improved social recognition abilities in oxytocin-deficient mice but not in oxytocin receptor knockout mice. The treatment reduced excessive neural activation following social stimulation and improved social recognition in environmentally-induced ASD model mice. The findings suggest KKT may work through oxytocin receptor pathways to normalize brain responses to social stimuli, though the mechanism requires further investigation.

While KKT shows promise for addressing social recognition deficits in animal models, extensive human trials are needed before clinical application. The oxytocin receptor dependency suggests potential biomarker-guided treatment approaches. Translation from animal models to human autism requires careful consideration of species differences.

Animal study only with no human data. Sample sizes not reported. Limited understanding of KKT's mechanism of action. Unclear generalizability to human autism. Single study without replication.

Kamikihito (KKT) is a traditional Japanese medicine used to treat insomnia, anemia, anxiety and neurosis. Its scientific mechanism of action is not well understood. This study aimed to evaluate the therapeutic effect of KKT on deficits in social recognition ability, a phenotype of autism spectrum disorder (ASD), and to investigate the involvement of oxytocin in its action. KKT was orally administered to wild-type (WT), Oxytocin knockout (Oxt (-/-)), and Oxt receptor knockout (Oxtr (-/-)) mice, and social recognition ability was assessed using a three-chamber test.

Neuronal activation changes in the brain after social stimulation were evaluated using c-Fos immunostaining in WT, Oxt (-/-), and Oxt (-/-) mice treated with KKT. Additionally, we examined whether KKT ameliorates social recognition impairment in LPS-induced ASD model mice (LPS mice), where LPS serves as an environmental factor. Abnormal social recognition behavior was improved in the Oxt (-/-) mice after sustained KKT administration, but not in the Oxtr (-/-) mice. c-Fos immunostaining revealed excessive neural activation of the Oxt (-/-) mice following social stimulation, which was reduced to WT levels after KKT administration. Social recognition impairment in the LPS mice was improved by KKT.

Our results suggest that KKT may improve social recognition by acting through Oxtr and by suppressing excessive neural activation after social stimulation. These effects may represent part of KKT's mechanism of action. It is possible for KKT to become a commonly used treatment for ASD-like symptoms.