Hypothalamic-Pituitary-Adrenal System

10 Key excerpts on "Hypothalamic-Pituitary-Adrenal System"

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  Child Psychopathology

  From Infancy to Adolescence

  • Barry H. Schneider(Author)
  • 2014(Publication Date)
  • Cambridge University Press

    (Publisher)

  Understanding the physiology of stress, therefore, is essential for understanding the biological basis of children’s emotional and behavioral maladjustment. The hypothalamic-pituitary-adrenal (HPA) axis The HPA axis system is considered to be one of the two principal stress response systems, along with the sympathetic-adrenomedullary system, which is discussed as part of autonomic physiology. The HPA axis functions through the coordinated activity of a series of organs within and outside the brain, which produce a cascade of hormones resulting in the release of cortisol from the adrenal glands ( Figure 5.4 ) (Gunnar and Adam, 2012 ; Kaltas and the production and regulation of human behavior. Hormones are chemicals secreted by neurons in various brain structures, such as the hypothalamus, and other organs, such as the adrenal glands, that circulate through cerebral spinal fluid and serum (blood) in order to affect the activity of other cells and organs. These chemical messengers are often thought of as the “slow road” to regulation: Whereas the autonomic nervous system – the “fast road” – can directly stimulate target organs in a matter of milliseconds to seconds, hormones can take several seconds to several minutes to produce their effects. Much like the proverbial tortoise and hare, however, it would be a mistake to discount the contributions of the slower participant in the race to regulate bodily processes. Hormones are vitally important messengers and triggers for physiological and behavioral activity, affecting metabolism, growth, immune functions, arousal states, mood and other functions. There are many hormones that affect human behavior and potentially are involved in emotional and behavioral problems.

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  Biological Psychiatry

  • Edward Bittar(Author)
  • 1999(Publication Date)
  • Elsevier Science

    (Publisher)

  Chapter 6 Psychological Aspects of H ypoth al am ic-P itu ita ry-Ad re nal Axis Activity EHUD UR Introduction Stress Stress and the Hypothalamo-Pituitary-Adrenal (HPA) Response Stimulus Parameters Individual Parameters Coping Social Parameters Limbic System and Hippocampus Corticotropin-Releasing Hormone (CRH) Hypothalamic CRH Behavioral Effects of CRH Arginine Vasopressin (AVP) AVP-Containing Pathways in the Hypothalamus 116 117 118 118 119 120 121 121 122 123 123 124 124 BiologicalPsychiatry,pages 115-133. Copyright 9 2000by JAI Press Inc. All rights of reproduction in any form reserved. ISBN: 1-55938-819-6 115 116 EHUD UR Behavioral Effects of AVP Adrenocorticotropic Hormone (ACTH) Regulation of ACTH Behavioral Effects of ACTH Cortisol and Cerebral Glucocorticoid Receptors Psychological Aspects of Endocrine Disorders of the HPA Axis Cushing's Syndrome Addison's Disease HPA Axis Disturbances in Neuropsychiatrie Disorders Major Depression Posttraumatic Stress Disorder Chronic Fatigue Syndrome Conclusions 124 124 124 125 126 126 126 127 128 128 129 130 130 INTRODUCTION The hypothalamo-pituitary-adrenal (HPA) axis plays a central role in the integra-tion of the response of the organism to stress. This is achieved through various homeostatic mechanisms controlling intermediary metabolism, blood pressure, and behavior. The neuroendocrine cascade triggered by stress begins with central perception of a stressor, thus leading to the release of corticotropin releasing hor-mone (CRH), arginine vasopressin (AVP), and other secretagogues for adreno-corticotrophin (ACTH). ACTH is released from the corticotrophic cells of the anterior pituitary, following posttranslational modification of its parent molecule proopiomelanocortin (POMC), and this peptide promotes the release of glucocorticoids from the adrenal gland. For technical reasons of accessibility, early work on the physiology of the HPA axis mostly concentrated on the distal effector limb of this cascade.

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  Integrative Therapies for Depression

  Redefining Models for Assessment, Treatment and Prevention

  • James M. Greenblatt, Kelly Brogan, James M. Greenblatt, Kelly Brogan(Authors)
  • 2015(Publication Date)
  • CRC Press

    (Publisher)

  171 12 The Hypothalamic-Pituitary-Adrenal Axis in Mood Disorders Sara Gottfried, MD INTRODUCTION We release hormones such as adrenaline and cortisol in response to stress—a smart evolutionary adaptation that triggers rapid physiologic changes such as increased heart rate and blood pressure, and redirects blood flow to your muscles so that you may fight or flee. For more than 50 years, sci-entists have agreed that psychosocial stressors are the most potent activators of the stress feedback loop, known as the hypothalamic-pituitary-adrenal (HPA) axis. 1 However, the alarm can backfire: CONTENTS Introduction .................................................................................................................................... 171 Normal Regulation of HPA Function ............................................................................................. 172 Allostatic Load ............................................................................................................................... 173 Pregnenolone Steal ......................................................................................................................... 173 HPA Dysregulation in Mood Disorders ......................................................................................... 173 General Adaptation Syndrome ....................................................................................................... 174 Evaluation of HPA ......................................................................................................................... 174 Gathering the Patient’s Story .................................................................................................... 174 Laboratory Investigation ........................................................................................................... 175 Summary of HPA Dysregulation in Mental Health .......................................................................

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  Psychoendocrinology

  • F. Robert Brush, Seymour Levine(Authors)
  • 2013(Publication Date)
  • Academic Press

    (Publisher)

  CHAPTER SEVEN

  Psychoneuroendocrinology of Stress: A Psychobiological Perspective

  Seymour Levine, Christopher Coe and Sandra G. Wiener

  Publisher Summary

  This chapter discusses specific psychological variables that are involved in the regulation of the Pituitary–Adrenal (P–A) activity and specific aspects of the psychological variables that can selectively affect and regulate the secretion of gonadal hormones. The influence of psychological factors on P–A hormones is bidirectional. The psychological stimuli not only participate in activating this system but also effectively inhibit it. This inhibition is manifested either by reduced elevations of plasma corticoids during aversive stimulation or by an actual decrease in circulating levels of corticoids. This effect is particularly pronounced when the predictable or reinforcing stimulus involves consummatory events. Apart from induced stress, feedback is another factor involved in this process. Feedback refers to stimuli or information occurring after a behavioral response has been made in reaction to an event. These stimuli may be used to convey information to the responding organism indicating that it has made the correct response to a noxious event. The field of neuroendocrinology has made tremendous advances in the past few decades in identifying many chemical substances that qualify as hormones not only in the pituitary and peripheral organs but also in the central nervous system.

  I Introduction

  Despite numerous and valiant attempts to define stress, a clear and universally accepted definition still remains, to say the least, elusive. It is not the purpose of this chapter, therefore, to dwell extensively on the problems related to the definition of stress. This would be an exercise in futility. It is important to note, however, that historically the concept of stress has always been associated with changes in the endocrine system. Initially, these changes were specifically related to either increased secretion of catecholamines or activation of the pituitary–adrenal (P–A) system. It has now been clearly demonstrated that many endocrine changes occur following those environmental events which are typically called stressful. The focus of a great deal of research related to stress physiology is still on the P–A system. It is, of course, impossible to discuss any facet of the P–A system and its relationship to environmental factors without acknowledging the landmark contributions of Hans Selye. His formulation of the General Adaptation Syndrome (GAS) highlighted the importance of this hormonal system and the diversive physiological effects of glucocorticoids following adverse stimulation (Selye, 1950

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  Stress, Neuropeptides, and systemic disease

  • James McCubbin(Author)
  • 2012(Publication Date)
  • Academic Press

    (Publisher)

  II Endocrine Regulation This page intentionally left blank 9 Stress, the Hypothalamic—Pituitary-Adrenal Axis, and Depression I. Introduction II. CRF and the Stress Response III. CRF and Depression IV. Summary References Control of the hypothalamic-pituitary-adrenal (ΗΡΑ) axis is a multistep integrated process involving several central nervous system sites (cerebral cortex, amygdala, locus ceruleus, hippocampus, etc.). Most, but perhaps not all, of these central inputs are eventually channeled to the hypothala-mus. In the hypothalamus these signals are transduced to humoral-type messages, release and release-inhibiting hormones, that are then released from nerve terminals in the eminence, the site of the primary plexus of the hypothalamo—hypophyseal-portal system. These hypothalamic hypophysi-otrophic hormones released from the hypothalamus travel a short distance to the anterior pituitary, where the signal is amplified and converted by the release of pituitary trophic hormones. The adrenohypophyseal hormones are then released into the general circulation, travel to their appropriate target organs, and effect a multitude of specific organ system responses. These responses are known to have major influences on blood pressure reg-ulation, reproductive function, and energy mobilization. In addition to the central control mentioned above, the various neuroendocrine axes are also influenced by a variety of feedback control loops. These feedback con-Stress, Neuropeptides, and Systemic Disease Copyright © 1991 by Academic Press, Inc. All rights of reproduction in any form reserved. James C. Ritchie Departments of Psychiatry and Pharmacology Duke University Medical Center Durham, North Carolina Charles B. Nemeroff Departments of Psychiatry and Pharmacology Duke University Medical Center Durham, North Carolina I. Introduction 181 182 James C. Ritchie and Charles B. Nemeroff trols can be of both a fast and slow nature and are known to involve both central and peripheral sites.

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  Neurobiology of Bipolar Disorder

  Road to Novel Therapeutics

  • Joao Quevedo, Andre Ferrer Carvalho, Eduard Vieta, Joao L. de Quevedo, Joao Luciano de Quevedo(Authors)
  • 2020(Publication Date)
  • Academic Press

    (Publisher)

  [4] . However, the role and entity of these alterations are yet to be determined, as well as whether the neuroendocrine dysfunction is one of the etiopathogenetic mechanisms behind these disorders or rather one of their manifestations. The aim of this chapter is to summarize literature findings up to date on the association between BD and the HPA axis. Since we will focus specifically on BD patients, the study of this relationship may be further complicated by several characteristics intrinsic to the disease, including the periodic clinical course, the symptomatological heterogeneity, and the obstacles in the diagnosis. We will start with an overview on what the HPA axis is and on its role in the stress response, then we will analyze the link with BD—also from a genetic perspective, finally discussing the potential clinical implications of such relationship.

  Hypotalamic-pituitary-adrenal (HPA) axis and stress response

  The HPA axis is the key hormonal mediator of the stress response. In stressful situations, cortical and subcortical centers modulate the activation of the paraventricular nucleus of the hypothalamus, which stimulates several neuroendocrine reactions, vital for the maintenance of homeostasis. The activation of the paraventricular nucleus (PVN) of the hypothalamus induces the release, among others, of corticotropin releasing hormone (CRH) in the pituitary portal system. CRH reaches the anterior pituitary gland and then stimulates the corticotropic cells to produce the prohormone proopiomelanocortin (POMC), which is cleaved to yield different peptides, including beta-endorphin, and the peptide hormones lipotropin, melanocyte-stimulating hormone, and adrenocorticotropic hormone (ACTH). ACTH is released from the pituitary gland in the systemic circle and reaches the adrenal cortex where it induces the production and secretion of glucocorticoids (GCs), mainly cortisol in humans. Plasma cortisol levels have a circadian rhythm that follows the secretion of ACTH, with the zenith in the morning (around 7 a.m.), a preprandial secretory peak, and an evening nadir (toward 8 p.m.).

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  Handbook of Psychophysiology

  • John T. Cacioppo, Louis G. Tassinary, Gary G. Berntson(Authors)
  • 2016(Publication Date)
  • Cambridge University Press

    (Publisher)

  Psychological challenges activate the HPA through top-down signals originating from forebrain structures, including the amygdala and prefrontal cortex (Brady, Porter, Conrad, & Mason, 1958; Davis, 2000; Lundberg & Frankenhaeuser, 1980; Mason, 1968; Rolls, 2015). This process is summarized in Figure 21.3. During periods of psychological stress, signals from the prefrontal cortex and limbic system act on the HPA and the SNS in parallel, releasing CORT and EPI into circulation (Figure 21.4). As a result, both arms of the stress endocrine system act in concert and reinforce one another. Hormone secretion during psychological stress results from a complex of CNS events including: (a) interactions between the prefrontal cortex and the amygdala during the appraisal process, (b) the resulting experience of emotion and initiation of behavioral coping, and (c) autonomic and endocrine outputs from the hypothalamus, along with (d) descending signals to the brainstem and spinal cord. In considering the initiation of psychological stress and its effects on the stress hormones, we have noted that Lazarus and Folkman (Folkman, 1984; Lazarus & Folkman, 1984) postulate primary and secondary apprai- sals of an event’s threat value and available coping resources. It is clear that these appraisals must involve interactions between the prefrontal cortex and the amyg- dala. The amygdala has extensive inputs from association areas of the cerebral cortex, and these convey sensory Tissues CORTISOL Adrenal Cortex Hypothalamus Paraventricular N. Ant. Pituitary ACTH CRF CRF AVP (– × 1) (– × 10) (–) Figure 21.2 The HPA and negative feedback loops. The release of CORT into the systemic circulation results in actions on periph- eral tissues and feedback to the pituitary and paraventricular nucleus of the hypothalamus. Here it exerts a greater negative feedback effect on CRF-only cells (–×10) and a much smaller effect on CRF/AVP cells (–×1). STRESS HORMONES IN PSYCHOPHYSIOLOGICAL RESEARCH 469

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  Environmental Illness

  Myth & Reality

  • Herman Staudenmayer(Author)
  • 2018(Publication Date)
  • Routledge

    (Publisher)

  The stress-response can account for multi-system complaints (Rose, 1980) and has been proposed as one psychogenic theory (Jewett, 1992a). This chapter focuses on central nervous system (CNS) complaints: difficulty concentrating, attentional difficulties, memory loss or poor memory, learning difficulties (inappropriately portrayed as dyslexia), difficulty expressing oneself or understanding others (portrayed as aphasia), feelings of being out of touch, depersonalization or derealization, fatigue, and irritability. These symptoms are what EI patients refer to collectively as “brain fog” or “brain fag”. They are mediated by disturbances of central neuronal pathways that regulate arousal, alertness, and vigilance, which in turn modulate the general capacity and effectiveness of cognitive processing involved in learning and memory (Craik and Lockhart, 1972; Ellis et al., 1984). These symptoms are also on the menu of criteria that define anxiety disorders, particularly panic attacks in DSM-IV.

  Chrousos and Gold (1992) described the three main physiologic systems involved in the stress-response: 1.  Corticotropin-releasing hormone (CRH), which affects the brain directly and also initiates a cascade of responses along the hypothalamic-pituitary-adrenal (HPA) axis 2.  Norepinephrine (NE) systems associated with the locus coeruleus (LC) referred to as LC-NE 3.  Autonomic nervous system (ANS), primarily the sympathetic branch.

  These three systems interact with inhibitory neurotransmitter systems to dampen the stress-response (Figure 9.1 ). They also interact with the endocrine and immune systems to create organ-specific and systemic effects. Each of these systems is defined with discussion focused on the stress-responses consistent with multi-system complaints seen in EI patients.

  Hypothalamic-pituitary-adrenal axis

  The HPA axis is the major neuroendocrine stress regulatory system in the body (Krishnan et al., 1991). Its clinical manifestations vary, depending on the extent and severity of the pituitary hormone deficiency and the specific organs targeted by the endocrine mediators. In the extreme, hypopituitarism may result from either pituitary or hypothalamic disease (Vance, 1994). Of note, dysregulation of the HPA-axis may result in nonspecific symptoms of fatigue and malaise.

  Corticotropin-releasing hormone (CRH) is a hypothalamic peptide widespread throughout the brain but best characterized in the hypothalamus, specifically in the paraventricular nucleus (PVN). In animal studies, exogenous stimulation with CRH has been associated with hypercortisolism, sympathetic activation, and behavioral activation and intense arousal (Sutton et al., 1982). Larger doses of CRH administered directly to the CNS produce effects that can be construed as frankly anxiogenic. This includes hyperresponsiveness to sensory stimuli, assumption of the freeze posture, decreased exploration in unfamiliar environments (avoidance), and enhancement of conditioned fear responses during aversive stimuli (Dunn and Berridge, 1990). In humans, parallel symptoms are defining of post-traumatic stress disorder (PTSD). For example, Vietnam combat veterans with PTSD have been found to have higher concentrations of cerebral spinal fluid CRH (Bremner et al., 1997).

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  Adrenal Toxicology

  • Philip W. Harvey, David J. Everett, Christopher J. Springall, Philip W. Harvey, David J. Everett, Christopher J. Springall(Authors)
  • 2008(Publication Date)
  • CRC Press

    (Publisher)

  Stress-Induced Activation of the HPA Axis The HPA axis plays a critical role in enabling the organism to prepare for, respond to, and cope with physical or psychological stress. The mechanisms by which different stresses promote the release of CRH and AVP are a subject of much current research as too are the processes which underlie the adaptive responses to repeated or chronic stress. Acute Stress It is now broadly established that stresses which have a psychological component use cortico-limbic pathways to drive the HPA response while those that are “phys-ical” in nature, e.g., hypotension, use the ascending noradrenergic pathways which project from the brain stem nuclei (A1 in the ventrolateral medulla and A2 in the nucleus tractus solitarius) to the PVN. This dogma is well supported by data from studies involving, for example, measurement of the stress-induced expression of the immediate early gene, c-fos , in discrete brain regions or of c-fos and CRH mRNAs in the PVN of animals in which the relevant ascending or descending neuronal inputs to the PVN have been lesioned surgically or pharmacologically. These studies have emphasized repeatedly the critical role of the amygdala, hip-pocampus, and bed nucleus stria terminalis in mediating the responses to acute psychogenic stressors (e.g., restraint), and the supporting roles of cortical regions, most notably the prefrontal and cingulate cortices. Among the most potent activators of the HPA axis are insults to the host defence system (e.g., infections and other immunological insults), which threaten the well-being of the organism. The mechanisms by which such assaults trigger the release of glucocorticoids have been hotly debated. Early studies exploring the responses to bacterial (injection of lipopolysaccharide, LPS) or viral (e.g., Newcastle disease) toxins pointed to cytokine-dependent mechanisms which trigger the release of CRH and, possibly, AVP from the hypothalamus (Sapolsky et al. , 1987).

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  Translational Pain Research

  From Mouse to Man

  • Lawrence Kruger, Alan R Light, Lawrence Kruger, Alan R Light(Authors)
  • 2009(Publication Date)
  • CRC Press

    (Publisher)

  Opioid medi- cations provide a strong example, as they resemble beta endorphin and other endog- enous opioids. The hypothalamo-pituitary-gonadal axis responds to such products as Painful Multi-Symptom Disorders 21 though they were endogenous signals and the result is often hypogonadism (Daniell, Lentz, and Mazer 2006). 1.5 DISTURBED INTERSUBSYSTEM COORDINATION Nervous, endocrine, and immune subsystems are interdependent and coordinate their response to a stressor. The connectivity essential for cross-subsystem coor- dination may falter or break down. Examples include the reciprocal relationship of cytokines with HPA axis regulation (Viveros-Paredes et al. 2006; Calcagni and Elenkov 2006; Rivest 2001; Dunn, Wang, and Ando 1999), the relationship of cytokine regulation to autonomic regulation (Czura and Tracey 2005), and the relationship of cytokine regulation to the LC response (Borsody and Weiss 2002). This is the mechanism for how dysregulation in one subsystem will tend to disrupt another, leading eventually to supersystem dysfunction. 1.5.1 INCOMPLETE STRESS RESPONSE RECOVERY Dysregulation could occur if a system alters its set point in response to a stressor and then fails to readjust to the normal level after the stress has passed. This corresponds with McEwen’s metaphor of failure to hear the all-clear signal (McEwen 2002). This explanatory model nicely describes the hypervigilance and hyperreactivity of post- traumatic stress disorder (Bedi and Arora 2007). Some multi-symptom syndrome patients have trauma histories. Set points are often straightforward to define. For example, Vogeser and col- leagues (Vogeser et al. 2003) studied major surgery as a stressor and chose the cortisol:cortisone ratio as a marker of HPA axis activity and as a stress-sensitive indi- cator of the overall set-point shift in the breakdown of cortisone to produce CORT, namely 11b-hydroxysteroid dehydrogenase activity.

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