Post‐traumatic stress disorder (PTSD) is a psychiatric disorder of high prevalence and major socioeconomic impact. Patients suffering from PTSD typically present intrusion and avoidance symptoms and alterations in arousal, mood and cognition that last for more than 1 month. Animal models are an indispensable tool to investigate underlying pathophysiological pathways and, in particular, the complex interplay of neuroendocrine, genetic and environmental factors that may be responsible for PTSD induction. Since the 1960s, numerous stress paradigms in rodents have been developed, based largely on Seligman's seminal formulation of ‘learned helplessness’ in canines. Rodent stress models make use of physiological or psychological stressors such as foot shock, underwater trauma, social defeat, early life stress or predator‐based stress. Apart from the brief exposure to an acute stressor, chronic stress models combining a succession of different stressors for a period of several weeks have also been developed. Chronic stress models in rats and mice may elicit characteristic PTSD‐like symptoms alongside, more broadly, depressive‐like behaviours. In this review, the major existing rodent models of PTSD are reviewed in terms of validity, advantages and limitations; moreover, significant results and implications for future research—such as the role of FKBP5, a mediator of the glucocorticoid stress response and promising target for therapeutic interventions—are discussed.

BackgroundOxytocin (OXT) is critically involved in the regulation of attachment and interpersonal function. In this study, emotional children’s movies were used to stimulate OXT secretion in patients with schizophrenia and healthy controls (HCs). Furthermore, associations of OXT levels with measures of attachment style (Psychosis Attachment Measure), childhood adversity (Childhood Trauma Questionnaire) and symptom severity [Positive and Negative Syndrome Scale (PANSS)] were considered.MethodsIn 35 patients with schizophrenia and 35 matched HCs, radioimmunoassay with sample extraction was used to determine OXT plasma levels before and after viewing of movie scenes portraying emotional bonding and loss and compared to a non-emotional condition.ResultsStatistical analysis indicated lower baseline OXT levels in female patients than in all other groups. OXT reactivity during emotional movies was significantly higher in patients when compared to HCs. OXT reactivity during the control movie related to PANSS `general psychopathology’. No significant associations appeared between baseline or induced OXT levels and other PANSS subscales, attachment style or childhood adversity in patients.ConclusionsOur findings suggest differences of baseline OXT and a higher OXT reactivity toward strong emotional stimuli in patients with schizophrenia, suggesting a role of OXT as a gender- and context-dependent modulator of socio-emotional function.

Microglia senescence may promote neuropsychiatric disease. This prompted us to examine the relationship between microglia activation states and telomere biology. A panel of candidate genes associated with telomere maintenance, mitochondrial biogenesis, and cell-cycle regulation were investigated in M1- and M2-polarized microglia in vitro as well as in MACS-purified CD11b+ microglia/brain macrophages from models of stroke, Alzheimer’s disease, and chronic stress. M1 polarization, ischemia, and Alzheimer pathology elicited a strikingly similar transcriptomic profile with, in particular, reduced expression of murine Tert. Our results link classical microglia activation with repression of telomere-associated genes, suggesting a new mechanism underlying microglia dysfunction.