Autism spectrum disorder (ASD) is rather common, presenting with prevalent early problems in social communication and accompanied by repetitive behavior. As vasopressin was implicated not only in salt-water homeostasis and stress-axis regulation, but also in social behavior, its role in the development of ASD might be suggested. In this review, we summarized a wide range of problems associated with ASD to which vasopressin might contribute, from social skills to communication, motor function problems, autonomous nervous system alterations as well as sleep disturbances, and altered sensory information processing. Beside functional connections between vasopressin and ASD, we draw attention to the anatomical background, highlighting several brain areas, including the paraventricular nucleus of the hypothalamus, medial preoptic area, lateral septum, bed nucleus of stria terminalis, amygdala, hippocampus, olfactory bulb and even the cerebellum, either producing vasopressin or containing vasopressinergic receptors (presumably V_1a). Sex differences in the vasopressinergic system might underline the male prevalence of ASD. Moreover, vasopressin might contribute to the effectiveness of available off-label therapies as well as serve as a possible target for intervention. In this sense, vasopressin, but paradoxically also V_1a receptor antagonist, were found to be effective in some clinical trials. We concluded that although vasopressin might be an effective candidate for ASD treatment, we might assume that only a subgroup (e.g., with stress-axis disturbances), a certain sex (most probably males) and a certain brain area (targeting by means of virus vectors) would benefit from this therapy.

People often turn to sweet foods for comfort during times of stress, as energy imbalance is implicated in several neuropsychiatric disorders including post-traumatic stress disorder (PTSD). Although acute sucrose consumption may improve cognitive capabilities, its long-term effectiveness has been debated. Objectives: In a widely used mouse model, we examined the effect of sucrose drinking on conditioned fear-induced freezing (as a model of PTSD), with emphasis on the concentrations and timing of the intervention as well as sex differences. We aimed to develop a low-cost, widely accessible therapeutic option. Methods: A short electric foot shock was used for trauma, and freezing was detected 24 h (mimicking acute stress disorder, ASD) or 14 days (PTSD-like symptoms) later in the trauma context and with trauma cues. Results: First, we confirmed that our trauma increased freezing, independent of previous habituation to sucrose drinking. Next, we confirmed that 16% and 32%, but not 2% sucrose drinking for 24 h (but not 3 h) immediately after trauma, diminished freezing behavior the next day. However, the same intervention did not influence behavior 14 days later. Moreover, we could not find any curative effect of 24 h of 16% sucrose consumption before testing remote fear memory 14 days after trauma. Conclusions: Consuming a high-calorie solution immediately following trauma for 24 h may influence ASD but does not necessarily alter the development of PTSD symptoms. Here, we offer a new perspective on energy regulation in neuropsychiatric disorders.