Neurobiologie

Exposure to early stressful adverse life events may increase vulnerability to psychopathology in adult life. There are important memory disturbances in stress-related psychiatric disorders. Therefore, there is much interest in understanding the mechanisms responsible for interactions between stress and cognition. Male Wistar rats that experienced 3-h daily separations from the dam during the first 3 weeks of life (maternal separation, MS) showed in adulthood a depressive-like behaviour in the forced swimming test, increased hypothalamic-pituitary-adrenal (HPA) axis responsiveness to stressors and elevated CRF mRNA in the paraventricular nucleus of the hypothalamus (PVN). In the hippocampus of MS rats, there was a lower glucocorticoid receptor density. MS produced significant learning impairments both in the Morris water maze and in the novel object recognition test (NORT). The glucocorticoid receptor antagonist mifepristone and the beta-adrenoceptor antagonist propranolol were able to completely reverse the increased immobility time in the forced swimming test and the memory deficits in the NORT observed in MS rats. Our data support the hypothesis that elevated secretion of glucocorticoids may be associated to behavioural and cognitive deficits in MS rats. The stress hyperresponsiveness observed in MS rats could be attributed, at least in part, to an impaired feedback sensitivity mediated by hippocampal glucocorticoid receptors. It can also be suggested the possible involvement of the noradrenergic system in cognitive impairments mediated by glucocorticoids in the MS model.

It is common for individuals with symptoms of posttraumatic stress disorder (PTSD) to present with co-occurring pain problems, and vice versa. However, the relation between these conditions often goes unrecognized in clinical settings. In this paper, we describe potential relations between PTSD and chronic pain and their implications for assessment and treatment. To accomplish this, we discuss phenomenological similarities of these conditions, the prevalence of chronic pain in patients with PTSD, and the prevalence of PTSD in patients with chronic pain. We also present several possible explanations for the co-occurrence of these disorders, based primarily on the notions of shared vulnerability and mutual maintenance. The paper concludes with an overview of future research directions, as well as practical recommendations for assessing and treating patients who present with co-occurring PTSD or chronic pain symptoms.

The effects on anxiety and risk assessment of exposure to a cat were tested in hooded rats. Anxiety and risk assessment were measured in an elevated plus maze and hole board in a room different from the cat-exposure room. Behavior was tested either 1, 2, 7, 14, or 21 days after cat exposure in different groups of rats. A single exposure to a cat increased anxiety over controls in the plus maze from 1 to 21 days after exposure to a cat. The effects on anxiety were independent of activity or exploratory tendency. Severity of anxiety produced was predicted by the approach, but not the attack, behavior of the cat. Analogous correlations between traumatic stimuli and anxiety are seen in humans suffering from posttraumatic stress disorder (PTSD). Risk assessment in the plus maze was reduced over the same period in rats exposed to cats. Risk assessment was weakly correlated with anxiety. The findings are discussed with respect to the potential of this phenomenon as a model of generalized anxiety disorder found in PTSD.