In the present study, we established and characterized an animal model of vulnerability to repeated stress. We found that control Sprague-Dawley (SD) rats showed a gradual decrease in the HPA axis response following 14 days of repeated restraint stress, whereas Fischer 344 (F344) rats did not show such HPA axis habituation. Similar habituation was observed in the expression of c-fos mRNA, corticotropin-releasing hormone hnRNA, and phospho-CREB and phospho-ERK proteins in the hypothalamic paraventricular nucleus (PVN) of SD rats, but not in the F344 rats. In addition, repeatedly restrained F344 rats exhibited decreased cell proliferation in the dentate gyrus of the hippocampus and increased anxiety-related behaviours, while repeatedly restrained SD rats exhibited a selective enhancement of hippocampal cell proliferation in the ventral area. Moreover, we found a lower expression of glucocorticoid receptor (GR) protein, but not mRNA, in the PVN of F344 rats compared to SD rats. We also identified that microRNA (miR)-18a inhibited translation of GR mRNA in cultured neuronal cells and that increased expression of miR-18a in the PVN was observed in F344 rats compared with SD rats. These strain differences in GR protein levels were not found in the hippocampus and prefrontal cortex, and the expression of miR-18a was much lower in these brain regions than in the PVN. Our results suggest that F344 rats could be a useful animal model for studying vulnerability to repeated stress, and that miR-18a-mediated down-regulation of GR translation may be an important factor to be considered in susceptibility to stress-related disorders.

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Although literature evidence suggests deficits in social and non-social cognition in patients with autistic spectrum disorder (ASD) and schizophrenia (SCZ), the difference in neural correlates of the impairments between the two disorders has not been elucidated. We examined brain function in response to a non-social cognition and a social cognition task using functional near-infrared spectroscopy (fNIRS) in 13 patients with ASD, 15 patients with SCZ, and 18 healthy subjects. We assessed the brain function of participants using a verbal fluency task and an emotional facial recognition task. The patients with ASD showed significantly reduced brain activation in the left frontotemporal area during both tasks compared to healthy subjects. The patients with ASD with larger score in ‘attention to detail’ in the autism spectrum quotient showed lower activation of the left frontotemporal area during the two tasks. The patients with SCZ showed significantly reduced activation, compared to healthy subjects, and greater activation, compared to patients with ASD, in the area during the verbal fluency task. The patients with SCZ with more severe symptoms had lower brain activation during the task in this area. Our results suggest that two distinct areas are involved in the distinctive brain pathophysiology relevant to cognitive processing in patients with ASD and SCZ.