The neuropeptide vasopressin influences different aspects of behavior, like emotions, anxiety, depression, memory, etc. Previous reports have suggested the participation of the vasopressinergic system in social behavior through the innervation of various nuclei of the brain, signaling through the V1a and V1b receptors. One of the mental disorders that sociability is affected is ASD, and some years ago, it was described as the participation of the vasopressin system in this disorder. The C58/J inbred mouse strain has a behavioral profile that reflects the core symptoms of autism, including deficits in sociability, impaired communication, and overt motor stereotypies. However, little is known about any anomaly in neuropeptide circuitry in these animals. To evaluate vasopressin's anatomic influence on ASD, we study the C58J strain, an animal model of ASD. Using immunohistochemistry to detect AVP, we found potentiated peptide and atypical innervation patterns in different nuclei, including the nucleus basalis of Meynert (NBM), the bed nucleus of stria terminals, and the medial amygdala. We used i.p. administration of a hypertonic saline solution (900 mM) and micro-positron emission tomography (micro-PET) technique to assess the functional consequence of this observed AVP system's potentiation. We found an increase in standardized uptake value (SUV) in the thalamus, hypothalamus, hippocampus, brain stem, central gray, superior colliculi, inferior colliculi, and midbrain after salt loading during which the hypothalamic AVP system is potently upregulated. Finally, we observed changes in the morphology and number of dendritic spines in the C58J strain compared to C57BL.