Recent studies revealed that the dysfunction of post-synapse and/or pre-synapse related to neuropsychological disorder such as autism spectrum disorders (ASD). HPC-1/syntaxin1A (STX1A) is known to regulate neurotransmitter release at pre-synaptic terminal. Previously, we found that some ASD patients were haploid for STX1A gene. We also reported that STX1A gene knockout mice (STX1A KO) showed unusual behavioral profiles similar to human ASD patient. Interestingly, the deficit of social recognition, one of the unusual behavior in STX1A KO, partially ameriolated with dopamine (DA) receptor agonist or oxytocin (OXT). We observed that the effect of OXT was suppressed by DA receptor antagonists, and the effect of DA was suppressed by OXT receptor antagonists. These results suggested the reciprocal interaction of DAergic and OXTergic system (OXT-DA interaction). We examined if OXT and DA modulated the respective secretion each other. In WT mice, OXT induced DA secretion, and DA induced OXT secretion. The both of DA and OXT secretion were suppressed in STX1A KO. These results indicated that disturbance of OXT-DA interaction possibly caused for the deficit of social recognition in STX1A KO. We also studied if glial cells contribute to the OXT-DA interaction. We observed that OXT receptors (OXTR, V1aR and V1bR) were expressed in the primary cultured WT glial cells derived from neonatal mice brain. In the cultured WT glial cells, WAY267464, an OXTR agonist, increased DOPAC/DA ratio. The effect of WAY267464 was partially suppressed L371,257, an OXTR antagonist, or SR490590, a V1aR antagonist. These observation suggested that OXTmodulate DA homeostasis in CNS.