Neuroendocrine Aspects of the Response to Stress

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Medical Abstract Title:

Neuroendocrine Aspects of the Response to Stress

Author:

DB, O'Callaghan JP.

Source:

Metabolism. 2002;51(6 Suppl 1):5-10.

Abstract:

Disruptions in homeostasis (ie, stress) place demands on the body that are

met by the activation of 2 systems, the hypothalamic-pituitary-adrenal (HPA)

axis and the sympathetic nervous system (SNS). Stressor-induced activation

of the HPA axis and the SNS results in a series of neural and endocrine

adaptations known as the " stress response " or " stress cascade. " The stress

cascade is responsible for allowing the body to make the necessary

physiological and metabolic changes required to cope with the demands of a

homeostatic challenge. Here we discuss the key elements of the HPA axis and

the neuroendocrine response to stress. A challenge to homeostasis (a

stressor) initiates the release of corticotropin-releasing hormone (CRH)

from the hypothalamus, which in turn results in release of

adrenocortiotropin hormone (ACTH) into general circulation. ACTH then acts

on the adrenal cortex resulting in release of a species-specific

glucocorticoid into blood. Glucocorticoids act in a negative feedback

fashion to terminate the release of CRH. The body strives to maintain

glucocorticoid levels within certain boundaries and interference at any

level of the axis will influence the other components via feedback loops.

Over- or underproduction of cortisol can result in the devastating diseases

of Cushing's and 's, respectively, but less severe dysregulation of

the HPA axis can still have adverse health consequences. These include the

deposition of visceral fat as well as cardiovascular disease (eg,

atherosclerosis). Thus, chronic stress with its physical and psychological

ramifications remains a persistent clinical problem for which new

pharmacological treatment strategies are aggressively sought. To date,

treatments have been based on the existing knowledge concerning the brain

areas and neurobiological substrates that subserve the stress response. Thus

the CRH blocker, antalarmin, is being investigated as a treatment for

chronic stress because it prevents CRH from having its ultimate effect-a

protracted release of glucocorticoids. New therapeutic strategies will

depend on the discovery of novel therapeutic targets at the cellular and

intracellular level. Advances in molecular biology provide the tools and new

opportunities for identifying these therapeutic targets.

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