Tussenbalans

Niet UB, maar tijdelijk ter bevordering van de PDF bestanden in het Leids Repositorium

Tussenbalans

Niet UB, maar tijdelijk ter bevordering van de PDF bestanden in het Leids Repositorium

Forced swim stressor: trends in usage and mechanistic consideration

The acquired immobility response during the "forced swim test (FST)" is not a rodent model of depression, but the test has some validity in predicting a compound's antidepressant potential. Nevertheless, 60% of the about 600 papers that were published annually the past 2 years label the rodent's immobility response as depression-like behaviour, but the relative contribution per country is changing. When the Editors-in-Chief of 5 journals publishing most FST papers were asked for their point of view on labelling immobility as depression-like behaviour and despair, they responded that they primarily rely on the reviewers regarding scientific merit of the submission. One Editor informs authors of the recent NIMH notice () which encourages investigators to use animal models "for" addressing neurobiological questions rather than as model "of" specific mental disorders. The neurobiological questions raised by use of the FST fall in two categories. First, research on the role of endocrine and metabolic factors, with roots in the 1980s, and with focus on the bottom-up action of glucocorticoids on circuits processing salient information, executive control and memory consolidation. Second, recent findings using novel technological and computational advances that have allowed great progress in charting top-down control in the switch from active to passive coping with the inescapable stressor executed by neuronal ensembles of the medial prefrontal cortex via the peri-aquaductal grey. It is expected that combining neural top-down and endocrine bottom-up approaches will provide new insights in the role of stress-coping and adaptation in pathogenesis of mental disorders.Diabetes mellitus: pathophysiological changes and therap

Stress and estrous cycle affect strategy but not performance of female C57BL/6J mice

Stress induces a switch in learning strategies of male C57BL/6J mice from predominantly spatial to more stimulus-response learning. To study generalization of these findings over sex, we investigated female C57BL/6J mice at three phases of the estrous cycle under non stress and acute (10 min) restraint stress conditions. On a circular hole board (CHB) task, about half of the naive female mice used spatial and stimulus-response strategies to solve the task. Under stress, female mice favored spatial over stimulus-response strategies, with 100% of female mice in the estrus phase. Performance expressed as latency to solve the task is only improved in stressed female mice in the estrus phase. We conclude that the use of learning strategies is influenced by sex and this difference between sexes is aggravated by acute stress

From Receptor Balance to Rational Glucocorticoid Therapy

Diabetes mellitus: pathophysiological changes and therap

Lifetime achievement from a brain-adrenal perspective: On the CRF-urocortin-glucocorticoid balance

Diabetes mellitus: pathophysiological changes and therap

From vasotocin to stress and cognition

Sex and stress hormones coordinate experience and behaviour with physiological regulations. In the brain the sex hormones act to promote the repertoire of affiliative and reproductive behaviours. Stress hormones target in particular brain circuits underlying emotional arousal and cognition. To exert these actions the hormones operate in concert with neuropeptide secreting systems. Here I will discuss three examples of hormone action on brain and behaviour. First in the song bird manipulation of brain vasotocin promotes acquisition of a stable stereotyped song pattern. Second in mammal's central glucocorticoid feedback action, initiated and enhanced by vasopressin, is mediated by two types of nuclear receptors that operate in complementary fashion to maintain homeostasis and health. One receptor system, the mineralocorticoid receptors, activates the switch from spatial to habit learning under stressful conditions, while the stress-induced behavioural response is stored in the memory via activation of the glucocorticoid receptors. Third, genetic predisposition and early life experience program neuropeptide and glucocorticoid systems for life with the goal to match with expected future demands. Hence, a mismatch between the early imprinted response modes with later life conditions enhances vulnerability to disease. These three topics have in common that they illustrate how hormones govern plasticity of neural stress circuitry underlying complex behavioural tasks, how upon dysregulation psychiatric disorders may develop for which the individual is predisposed and how such hormone action may promote resilience still present in the diseased brain. (C) 2009 Elsevier B.V. All rights reserved.Stress hormones and brain functio