Stress: Neuroendocrinology and Neurobiology

Handbook of Stress Series, Volume 2

George Fink

• Publisher: Academic Press
• Year: 2016
• Print ISBN: 9780128021750
• eBook ISBN: 9780128024232
• Topic: Medicine
• Subtopic: Endocrinology & Metabolism

Stress: Neuroendocrinology and Neurobiology: Handbook of Stress Series, Volume 2, focuses on neuroendocrinology, the discipline that deals with the way that the brain controls hormonal secretion, and in turn, the way that hormones control the brain. There have been significant advances in our understanding of neuroendocrine molecular and epigenetic mechanisms, especially in the way in which stress-induced hormonal and neurochemical changes affect brain plasticity, neuronal connectivity, and synaptic function. The book features the topic of epigenetics, and how it enables stress and other external factors to affect genetic transmission and expression without changes in DNA sequence. Integrated closely with new behavioral findings and relevance to human disorders, the concepts and data in this volume offer the reader cutting-edge information on the neuroendocrinology of stress. Volume 2 is of prime interest to neuroscientists, clinicians, researchers, academics, and graduate students in neuroendocrinology, neuroscience, biomedicine, endocrinology, psychology, psychiatry, and in some areas of the social sciences, including stress and its management in the workplace. - Includes chapters that offer impressive scope with topics addressing the neuroendocrinology and endocrinology of stress - Presents articles carefully selected by eminent stress researchers and prepared by contributors that represent outstanding scholarship in the field - Richly illustrated, with explanatory figures and tables

Part I

Neuroendocrine Control of the Stress Response

Outline

Chapter 1. Stress Neuroendocrinology: Highlights and Controversies

Chapter 2. Limbic Forebrain Modulation of Neuroendocrine Responses to Emotional Stress

Chapter 3. Adrenergic Neurons in the CNS

Chapter 4. Noradrenergic Control of Arousal and Stress

Chapter 5. Evolution and Phylogeny of the Corticotropin-Releasing Factor Family of Peptides

Chapter 6. Corticotropin-Releasing Factor and Urocortin Receptors

Chapter 7. Tracking the Coupling of External Signals to Intracellular Programs Controlling Peptide Synthesis and Release in Hypothalamic Neuroendocrine Neurons

Chapter 8. Neural Circuitry of Stress, Fear, and Anxiety: Focus on Extended Amygdala Corticotropin-Releasing Factor Systems

Chapter 9. Vasopressin as a Stress Hormone

Chapter 10. Adrenocorticotropic Hormone

Chapter 11. The Role of MicroRNAs in Stress-Induced Psychopathologies

Chapter 12. Stress Reactions Orchestrate Parasympathetic Functioning and Inflammation Under Diverse Cholinergic Manipulations

Chapter 13. Early Life Stress- and Sex-Dependent Effects on Hippocampal Neurogenesis

Chapter 14. Stress, Alcohol and Epigenetic Transmission

Chapter 15. Stress, Panic, and Central Serotonergic Inhibition

Chapter 16. Neuroendocrinology of Posttraumatic Stress Disorder: Focus on the HPA Axis

Chapter 17. Stress and Major Depression: Neuroendocrine and Biopsychosocial Mechanisms

Chapter 18. Telomeres and Early Life Stress

Chapter 1

Stress Neuroendocrinology

Highlights and Controversies

G. Fink University of Melbourne, Parkville, VIC, Australia

Abstract

Stress in mammals triggers a neuroendocrine response mediated by the hypothalamic–pituitary–adrenal (HPA) axis and the autonomic nervous system (ANS). Increased activity of these two systems induces behavioral, cardiovascular, endocrine, and metabolic cascades that enable the individual to fight or flee and cope with stress. Our understanding of stress and stress response mechanisms is generally robust. However, several themes remain uncertain/controversial and perhaps deserve further scrutiny before they achieve canonical status. These themes include perinatal exposure effects on the health of the adult, genetic susceptibility to stress, the neurochemistry of posttraumatic stress disorder (ANS versus the HPA), significance of hippocampal volume for major depressive disorder and other mental disorders, and the role of stress in the etiology of gastroduodenal ulcers. All five themes are of clinical and therapeutic significance, pose fundamental questions about stress mechanisms and offer important areas for future research.

Keywords

Amygdala; Arginine vasopressin (AVP); Autonomic nervous system; Bipolar disorder; Catecholamines; Corticosterone; Corticotropin releasing factor (CRF); Cortisol; Dexamethasone; Dopamine; Epinephrine; Gastroduodenal ulcers; Gene × environment; Glucocorticoids; Hippocampus; Hypophysial portal vessels; Hypothalamic–pituitary–adrenal (HPA) axis; Major depressive disorder (MDD); MPTP; MRI; Neurohormones; Norepinephrine; Posttraumatic disorder (PTSD); Prefrontal cortex; Schizophrenia; Serotonin; Serotonin transporter (SERT); Sympatho-adrenomedullary system

Outline

Introduction

Neuroendocrine and Autonomic Nervous Control of Stress Response

Thrifty Phenotype Hypothesis: Variance Between Studies and Broadened to Include Maternal Obesity and Diabetes

Genetic Susceptibility to Stress: Gene × Environment Interaction

Posttraumatic Stress Disorder: Autonomic Nervous System Apparently Dominant

Neuroendocrine Correlates: No Consistent Evidence for Hypocortisolemia in Posttraumatic Stress Disorder

Autonomic Nervous System Correlates of PTSD: Robust Evidence for Increased Sympathetic Activity and Arousal in PTSD

Conclusions

Human Hippocampus and Major Depressive Disorder: Does Hippocampal Size Matter?

Background to Hippocampal Volume Reduction in Major Depressive Disorder

Magnetic Resonance Imaging Findings in Conflict

Mechanisms of Hippocampal Volume Changes and Reversibility

Impact of Normal Variability of Hippocampal Volume

Functional Changes and Relevance for Cognition and Dementia

Lack of Illness Specificity

Conclusions

Gastroduodenal (Peptic) Ulcers: Stress–Helicobacter pylori Interactions

General Conclusions and Observations

Acknowledgments

References

Key Points

• Stress in mammals triggers a neuroendocrine response mediated by the hypothalamic–pituitary–adrenal (HPA) axis and the autonomic nervous system (ANS).

• Increased activity of these two systems induces behavioral, cardiovascular, endocrine, and metabolic cascades that enable the individual to fight or flee and cope with stress.

• Our understanding of stress and stress response mechanisms is generally robust. However, several themes remain uncertain and/or controversial and deserve further scrutiny before they achieve canonical status.

• These themes include:

• The “thrifty phenotype hypothesis” and other perinatal factors such as maternal obesity and diabetes that may adversely affect health in adult life;

• Genetic susceptibility (gene × environment interactions) to stress, which is at an early stage of development;

• The neurochemistry of posttraumatic stress disorder (PTSD)…nearly three decades of research suggest that the ANS plays a dominant and more consistent role in PTSD than the HPA axis;

• Significance of hippocampal volume for major depressive and other mental disorders…the weight of evidence suggests that changes in hippocampal volume are reversible and a function of state rather than trait;

• Notwithstanding the importance of Helicobacter pylori, stress (especially trauma and burns) plays an important role in the etiology of gastroduodenal ulcers.

• All five themes are of clinical and therapeutic significance, pose fundamental questions about stress mechanisms, and offer important areas for future research.

Introduction

Stress concepts, definitions, and history have been covered in Volume 1 of this Handbook Series and in numerous reviews.^1–3 Briefly, the two founders of stress concepts, mechanisms, and impact were Walter Bradford Cannon at Harvard and Hans Selye at McGill. Cannon⁴ introduced the phrase “fight or flight” and showed how these responses to a stressful challenge were dependent on activation of the sympatho-neuronal and sympatho-adrenomedullary systems (SAS). Cannon also introduced the concept of homeostasis. Based on observations in humans and experimental animals, Hans Selye advanced the first, generic definition of stress: “Stress is the non-specific response of the body to any demand.”^5,6 Although criticized by some because of the claim of nonspecificity, Selye’s definition applies to all known stress responses in the three major phylogenetic domains.¹

Selye was also the first to recognize that homeostasis, “stability through constancy,” could not by itself ensure stability of body systems under stress. He coined the term heterostasis (from the Greek heteros or other) as the process by which a new steady state was achieved by adaptive mechanisms. Heterostasis, could be regarded as the precursor for the concept of allostasis, “stability through change” brought about by central neural regulation of the set points that adjust physiological parameters to meet the stressful challenge. Allostasis^7–9 has partly overtaken homeostasis, “stability through constancy” that dominated physiological and medical thinking since the 19th century influenced, for example, by Claude Bernard’s precept of the “fixity of the milieu interieur.”¹⁰

This second volume of the Handbook of Stress Series is focused on the neuroendocrine, autonomic nervous, and other neurobiological systems/mechanisms involved in the stress response. Because the d...

Table of contents

• Cover image
• Title page
• Table of Contents
• Copyright
• List of Contributors
• Preface
• Part I. Neuroendocrine Control of the Stress Response
• Part II. Endocrine Systems and Mechanisms in Stress Control
• Part III. Diurnal, Seasonal, and Ultradian Systems
• Index