The neuroendocrinology of depression and chronic stress

Abstract

This chapter will review basic and clinical studies of the social, genetic and developmental influences upon the reactivity of the hypothalamic pituitary adrenal (HPA) axis and the relationship of these to depression. Significant advances have taken place in each of these areas and it is now possible to interlink many of these areas of work. In order to do so, this chapter will be organised into five sections.The first section will show how the neuroendocrinology of chronic stress is characterised by an up-regulation of the central drive to the HPA axis in conjunction with downregulation of its negative feedback control.The second will show that very similar processes occur in depressive illness.The third section will describe social, developmental and genetic influences on the HPA axis both in experimental animals and in man.The fourth will show how activation of the HPA axis can influence the development of animal models of depression as well as the onset and perpetuation of clinical depression.The final section will draw together an overall hypothesis and indicate the potential for new treatments for depression that arise from this work. The neuroendocrinology of acute and chronic stressThe secretion of corticosteroid hormones (predominantly cortisol in man and corticosterone in the rat) is the most important endocrine component of the response to stress and the one that is most necessary for successful adaptation: the acute response has a time course of 1-2 h and the chronic response one of days or weeks. HPA activation in response to acute stress -animal studiesThe central drive to the stress response of the HPA axis is organised by the parvocellular component of the paraventricular nucleus (PVN) of the hypothalamus. Some of these cells synthesise corticotropin releasing Postal address: hormone (CRH) alone and some both CRH and arginine vasopressin Prof Stuart chockley, (AVP), but both types of cells project to the external zone of the median institute of Psychiatry, eminence and release their hormones into the hypophyseal portal system Denmark HiTLndo'n wm ch carries the hormones to the anterior pituitary gland. In response to SE5 8AF, UK an acute stress there is an increase in the synthesis of CRH mRNA and

Nutritional influences on cognitive function: mechanisms of susceptibility

“…No mood measures were reported in that study, but chronically high cortisol has frequently been linked to dysphoric mood and clinical depression (Checkley, 1996), although this might relate to dysfunction of brain 5-HT systems as well as the hypothalamic pituitary adrenal axis (Van Praag, 1996). Indeed, high baseline plasma cortisol predicts induction of depression by acute dietary TRP depletion (Åberg-Wistedt et al 1998).…”

Vascular depression in older people with diabetes

“…Potential causes of depression in chronic disease include psychosocial factors related to the burden of disease [9] and/or pathophysiological changes in neuroendocrine or immune function [10,11]. In addition, late-life cerebrovascular disease may predispose to or precipitate depression [12][13][14].…”

O eixo hipotálamo-pituitária-adrenal, a função dos receptores de glicocorticóides e sua importância na depressão

“…Of all endocrine axes, the hypothalamic-pituitary-adrenal (HPA) axis has been the most widely evaluated. 1,2 The HPA axis plays a fundamental role in the response to external and internal stimuli including psychological stressors. Abnormalities in the function of the HPA axis have been described in people experiencing psychiatric disorders.…”

“…Moreover, is well known the fundamental role of stress in precipitating episodes of psychiatric disorders in predisposed individuals. 1 These abnormalities seem related to changes in the ability of circulating glucocorticoids to exert their negative feedback on the secretion of HPA hormones through binding to the mineralocorticoid receptor (MR) and the glucocorticoid receptor (GR) in HPA tissues. 2,3,6 In fact, previous studies have described both an impaired HPA negative feedback, leading to hypercortisolemia, as in melancholic depression.…”