Neuroendocrinology of Stress PDF

Neuroendocrinology of Stress PDF



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Preface

A common feature of various definitions of stress, as experienced by people and animals, is a change in the internal or external environment that threatens homeostasis, in a way that may endanger survival or lead to ill-health. From the earliest formulation of concepts of stress it has been convincingly established that central to automatic physiological coping responses to stressful stimuli (stressors) are the sympathetic–adrenomedullary (SAM) and hypothalamic–pituitary–adrenocortical (HPA) neuroendocrine systems. The rapid responses of these systems liberate into the circulation biologically powerful chemicals, respectively catecholamines and glucocorticoids, and these hormones have bodywide actions to mobilize energy, increase blood flow to essential organs and to optimize brain activity to deal with the emergency. Because these hormones are so powerful, with deleterious actions when high levels are maintained, it is advantageous to restore the stress-induced secretion back to normal basal activity when the danger has passed.
The chapters in this book aim to highlight current knowledge of the organization and physiology of these stress response systems, how the impact of dysregulation of these systems is being investigated and to consider ways in which contributions to both psychiatric and physical diseases as a result of chronic stress effects on HPA axis function, in particular, can be critically addressed in basic research. Chapters have been organized in a sequence that starts with analysis of mechanisms in the key nodes in the adrenomedullary and HPA responses to stress, using animal and human models. The next chapters move on to consider how animal models are being used to address human stress-related disorders, while the final chapters focus on the programming by early-life experiences of HPA axis stress responsiveness and the process of drug design and testing aimed at specific molecular targets important in modulating stress responses.
Chapters 1 and 2 show how it has become clear that the activity of the HPA axis is controlled by multiple interconnected central neural networks and that different types of stressor are processed by anatomically and neurochemically distinct networks, predominantly aminergic or catecholaminergic, converging on to corticotropin releasing factor/hormone (CRF/CRH neurons in the hypothalamus) and regulating sympathetic nervous system output. These circuits both provide feedforward control, via inhibitory and excitatory inputs to CRF/CRH neurons, and mediate glucocorticoid negative feedback inhibition, which can be rapid via membrane receptors. Plasticity or adaptation of the elements of the HPA axis is a feature of chronic stress, and the synaptic and cellular mechanisms in CRF/CRH neurons, hippocampus and amygdala are being uncovered with electrophysiological techniques (Chapter 3). A similar approach, combined with modelling of electrophysiological properties is revealing details of how secretion of ACTH by anterior pituitary cells is triggered (Chapter 4). Complementary gene expression studies on chromaffin cells in the adrenal medulla reveal profound plasticity in these cells, as a result of even acute as well as chronic stress, which sustains adrenaline production (Chapter 5). In Chapter 6, human studies involving brain imaging and physiological readouts of autonomic responses that have validated animal studies of stress circuitry are detailed; these are providing new insights into the distinct importance of responses of the SAM and HPA axes in the perception of stress.


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