Neuroendocrinology of Stress 1st Edition by John Russell, Michael Shipston 1119951704 9781119951704

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ISBN 10: 1119951704

ISBN 13: 9781119951704

Author: John A. Russell, Michael J. Shipston

Exposure to chronic stress has cumulative adverse effects on physical and mental health, considered to be the consequence of chronic exposure to high levels of stress hormones. Consequently, there is extensive research in progress to investigate and better understand how the brain organises neuroendocrine stress responses and how interventions may be able to moderate these responses to improve mental and physical health. Neuroendocrinology of Stress  highlights current knowledge of the organisation and physiology of these stress response systems, how the impact of dysregulation of these systems is being investigated, and considers the ways in which contributions to both psychiatric and physical diseases resulting from chronic stress effects can be critically addressed in basic research Written by a team of internationally renowned researchers, each chapter presents a succinct summary of the very latest developments in the field Both print and enhanced e-book versions are available Illustrated in full colour throughout This is the second volume in a new Series “Masterclass in Neuroendocrinology”, a co- publication between Wiley and the INF (International Neuroendocrine Federation) that aims to illustrate highest standards and encourage the use of the latest technologies in basic and clinical research and hopes to provide inspiration for further exploration into the exciting field of neuroendocrinology.

Neuroendocrinology of Stress 1st Table of contents:

Chapter 1 Methods and Approaches to Understand Stress Processing Circuitry

1.1 Introduction

1.2 Assessment of stress activation

1.2.1 Markers of acute activation: Fos

1.2.2 Markers of acute activation: phosphorylated transcription factors

1.2.3 Assessing chronic activation: deltaFosB

1.3 Stress circuit connectivity

1.3.1 Anterograde tracing

1.3.2 Retrograde tracing

1.3.3 Combined anterograde and retrograde tracing

1.4 Lesion, inactivation and stimulation approaches

1.4.1 Lesion studies

1.4.2 Inactivation/activation studies

1.4.3 Optogenetics and DREADDs

1.4.4 Genetic models

1.5 Perspectives

Cited references

Chapter 2 Brain Monoaminergic Systems in Stress Neuroendocrinology

2.1 Introduction

2.1.1 Fundamentals of the hypothalamic-pituitary-adrenal axis

2.2 Serotonergic systems and HPA axis function

2.2.1 Neuroanatomy of serotonergic systems and the HPA axis

2.2.2 Serotonin neurochemistry and neuropharmacology in the PVN

2.2.3 Serotonergic systems and negative feedback control of the HPA axis

2.2.4 Genetics of serotonergic systems and the HPA axis function

2.2.5 Development and serotonergic control of HPA axis function

2.3 Catecholaminergic systems and HPA axis function

2.3.1 Norepinephrine/epinephrine

2.3.2 Dopaminergic systems and HPA axis function

2.4 Histaminergic systems and HPA axis function

2.5 Organic cation transporters and monoaminergic control of the HPA axis

2.6 Conclusions/implications

Cited references

Chapter 3 The Synaptic Physiology of the Central Nervous System Response to Stress

3.1 The hypothalamic-pituitary-adrenal axis

3.2 Corticosteroid signalling: Mineralocorticoid and glucocorticoid receptors

3.3 Electrophysiology of hypothalamic circuits controlling the HPA axis

3.3.1 Circadian activation of the HPA axis

3.3.2 Stress activation of the HPA axis

3.3.3 Glutamate and GABA synaptic regulation of CRH neurons

3.3.4 Noradrenergic regulation of CRH neurons

3.3.5 Stress plasticity of synaptic circuits controlling the HPA axis

3.3.6 Glucocorticoid negative feedback

3.4 Electrophysiological responses of hippocampal cells to stress

3.4.1 Organization of the hippocampal formation

3.4.2 Rapid changes in hippocampal cell function during the stress response

3.4.3 Delayed effects on hippocampal cell function following the stress response

3.5 Electrophysiological responses of amygdala cells to stress

3.5.1 Organization of the amygdala in relation to stress

3.5.2 Rapid changes in amygdala cell function during the stress response

3.5.3 Delayed effects of stress on the amygdalar cell function

3.6 Perspective

3.6 Acknowledgements

Cited references

Chapter 4 Illuminating the (Electro)physiology of Anterior Pituitary Corticotrophs

4.1 Introduction: Stress and the pivotal role of the anterior pituitary corticotroph

4.1.1 Hypothalamic neuropeptides stimulate corticotrophs to release ACTH

4.1.2 CRH and AVP activate distinct G-protein coupled receptors (GPCRs) to stimulate ACTH release

4.1.3 Glucocorticoid negative feedback

4.1.4 Role of ion channels in corticotroph physiology

4.2 How to identify a living corticotroph?

4.2.1 Previous models and approaches to identify corticotrophs

4.2.2 Developing a labelling approach using lentivirus

4.3 Exploiting labelled corticotrophs to explore ion channels and excitability

4.3.1 Corticotrophs display heterogeneous spontaneous excitability

4.3.2 A TTX-insensitive Na+ conductance controls resting membrane potential

4.3.3 CRH and AVP depolarize corticotrophs and stimulate a sustained increase in excitability

4.3.4 SK4 channels are a major component of outward K conductance

4.3.5 Labelling allows corticotroph transcriptome to be interrogated

4.4 Modelling corticotroph excitability

4.4.1 Building the model

4.4.2 Model equations for KIR, NaNS and KA

4.4.3 Modelling excitability in murine corticotrophs

4.5 Discussion

4.5.1 Pros and cons of lentiviral mediated corticotroph labelling

4.5.2 What have we learnt from ‘illuminating’ corticotrophs?

4.5.3 Opportunities for exploiting lentiviral transduced corticotrophs

4.5.4 Development of, and predictions from, the corticotroph excitability model

4.6 Perspectives

Cited references

Chapter 5 Stress and Sympathoadrenomedullary Mechanisms

5.1 Stress and research on stress

5.1.1 Definition of stress

5.1.2 Types of stressors

5.1.3 Studies on neuroendocrine stress mechanisms

5.2 Stress-triggered adrenomedullary catecholamine release

5.2.1 Stress-triggered catecholamine release and actions

5.2.2 Vesicular storage and quantal release of catecholamines

5.2.3 Gap junctions and chromaffin cell-cell communication

5.3 Stress-triggered induction of catecholamine biosynthesis

5.3.1 Changes in catecholamine synthesizing enzyme activity and expression

5.3.2 Acute versus repeated stress

5.3.3 Sensitization to a novel, heterotypic, stressor

5.3.4 Conclusions from chronic stress studies

5.4 Transcriptional pathways associated with acute and repeated stress

5.4.1 Synthesizing gene promoter regulation

5.5 Effects of stress on adrenomedullary peptide gene expression

5.5.1 Stress and adrenal proenkephalin

5.5.2 Stress and adrenal neuropeptide Y

5.5.3 Stress and adrenal urocortin 2 and the corticotropin releasing hormone (CRH) family of peptide

5.6 Microarray analysis of stress-triggered changes in gene expression in adrenal medulla

5.7 Neuronal, hormonal or humoral inputs for regulation of catecholamine biosynthesis and release

5.7.1 Splanchnic nerve input

5.7.2 HPA axis

5.7.3 The renin-angiotensin system (RAS) and the kallikrein-kinin system

5.8 Prospective

5.8 Acknowledgements

Cited references

Chapter 6 Neuroendocrine Mechanisms of Stress Regulation in Humans

6.1 A short account of stress research concepts

6.2 Systems associated with stress

6.2.1 Autonomic nervous system

6.2.2 Hypothalamus-pituitary-adrenal axis

6.2.3 SNS and HPA response times

6.2.4 Activation of the HPA axis with stress

6.2.5 Psychological perspective

6.3 Measures of stress

6.3.1 Psychological stress state

6.3.2 Sympathetic nervous system activity

6.3.3 HPA axis activity

6.3.4 Immune system responses to stress

6.4 The interaction of the stress response systems and the relevance for (psycho)pathology

6.4.1 HPA, SNS and psychological stress response interactions

6.4.2 Experimental separation of the neuroendocrine stress response systems

6.4 Summary and outlook

Cited references

Chapter 7 Studying Chronic Stress in Animals: Purposes, Models and Consequences

7.1 Introduction

7.1.1 Physical and emotional stressors

7.1.2 Chronic stress models

7.2 Adaptation to stressors repeated daily

7.2.1 Physical stressors

7.2.2 Emotional stressors

7.2.3 Central mechanisms of adaptation

7.3 Overall neuroendocrine consequences of daily exposure to stressors

7.3.1 General approach

7.3.2 Chronic intermittent exposure to severe stressors

7.3.3 Social stress

7.3.4 Other neuroendocrine systems involving anterior pituitary hormones

7.4 Conclusions and perspectives

Cited references

Chapter 8 Modelling Stress-Related Mood Disorders in Animals

8.1 Stress-related mood disorders

8.1.1 Mood disorders

8.2 Animal models for stress-related mood disorders

8.2.1 Why is it necessary to include animal studies in research of mental disorders?

8.2.2 To what extent can stress-related mood disorders be modelled in animals?

8.2.3 Limitations of rodent models

8.2.4 Validity criteria for animal models of stress-related mood disorders

8.2.5 Stress models of depression

8.3 Tests for assessing symptoms of depression in rodents

8.3.1 Tests for depression-like symptoms

8.3.2 Additional variables supporting a depression-related phenotype

8.4 Mechanisms of mood disorders: Contributions from animal models

8.4.1 Depression and monoamines

8.4.2 Depression and glutamate

8.4.3 Depression and neurotrophic factors

8.4.4 Depression and neuropeptides

8.4.5 Depression, HPA axis function and epigenetics

8.5 Perspectives

Cited references

Chapter 9 Glucocorticoid Involvement in Drug Abuse and Addiction

9.1 Drug addiction

9.1.1 Societal impact and need for treatment

9.1.2 Addiction as a neuroplasticity-related disease

9.2 Stress, motivation and addiction

9.2.1 Stress and motivational systems

9.2.2 Stress and addiction

9.3 Glucocorticoids and addiction

9.3.1 Overview of glucocorticoid actions

9.3.2 Glucocorticoid regulation of motivational systems

9.3.3 Mechanisms of glucocorticoid action

9.4 Cocaine: Mechanism of action

9.5 The rat intravenous (i.v.) drug self-administration approach for the study of drug abuse/addicti

9.6 Preclinical assessment of the involvement of glucocorticoids in addiction

9.6.1 Acquisition of self-administration

9.6.2 Maintenance of self-administration

9.6.3 Reinstatement of drug-seeking behaviour

9.6.4 Escalation of drug use

9.6.5 Effects of long-access cocaine self-administration on reinstatement

9.7 Glucocorticoid-dependent neuroplasticity that contributes to addiction

9.7.1 CRF systems and cocaine-induced neuroplasticity

9.7.2 Glucocorticoid regulation of neuroplasticity in CRF systems

9.8 Effects of cocaine self-administration on glucocorticoids

9.8.1 Human studies

9.9 Similarities and differences in glucocorticoid contributions across classes of illicit drugs

9.10 Summary

Cited references

Chapter 10 The Hypothalamic-Pituitary-Adrenal Axis: Circadian Dysregulation and Obesity

10.1 Historical introduction

10.1.1 Circadian rhythms

10.1.2 Suprachiasmatic nucleus – the master clock

10.1.3 SCN projections

10.1.4 Importance of HPA axis rhythms

10.2 The daily cortisol/corticosterone rise

10.2.1 Activation of glucocorticoid secretion on waking up

10.2.2 Cortisol awakening response (CAR)

10.3 Circadian rhythms in the hypothalamic-pituitary-adrenal axis

10.3.1 HPA axis control by paraventricular nucleus

10.3.2 Inhibitory role of vasopressin from SCN neurons

10.3.3 Non-ACTH regulation of adrenal cortex

10.4 The food-anticipatory rise in corticosterone secretion

10.4.1 Discovery of the phenomenon

10.4.2 Neural mechanisms

10.5 Clock gene rhythms within the adrenal gland

10.5.1 Evidence for adrenal rhythms

10.5.2 Clock genes in the adrenal glands

10.5.3 Control of adrenal clocks

10.5.4 Role of adrenal oscillator

10.5.5 Conclusions

10.6 Entrainment of peripheral clocks by glucocorticoids

10.6.1 Involvement of receptors for glucocorticoids in the brain

10.6.2 Regulation of peripheral clocks by glucocorticoids

10.6.3 Glucocorticoids and behavioural rhythms

10.7 Glucocorticoids and the metabolic syndrome

10.7.1 Metabolic actions of glucocorticoids

10.7.2 Obesity and glucocorticoids

10.7.3 Stress and eating

10.7.4 HPA axis gene variation and obesity

10.7.5 Structural brain changes in obesity

10.7.6 Stress and visceral obesity

10.8 Shift work and adrenal corticoids

10.8.1 Does shift work shift the daily cortisol rhythm?

10.8.2 Circadian clock, aldosterone and hypertension

10.9 Conclusions

10.9 Acknowledgements

Cited references

Chapter 11 Using Rodent Models to Explore the Role of 11β-HSD2 in Prenatal Programming by Glucocort

11.1 Developmental programming

11.1.1 Glucocorticoids as a central mediator of developmental programming

11.1.2 Feto-placental 11β-HSD2: A barrier against excess glucocorticoid exposure

11.1.3 Human epidemiological evidence for central programming

11.1.4 Modelling the epidemiological evidence with animal models

11.2 11β-HSD2: The epicentre of developmental programming?

11.2.1 What can influence 11β-HSD2 levels and how?

11.2.2 Transgenic mouse models of altered 11β-HSD2 function

11.2.3 How are 11β-HSD2 knock-out mice ‘feeling’?

11.3 How might deletion of 11β-HSD2 programme affective behaviour?

11.3.1 Influence on the HPA axis

11.3.2 Influence on the developing monoaminergic system

11.3.3 Influence on brain structure

11.4 Don’t forget the placenta!

11.4.1 Is placental vasculature altered?

11.4.2 Is placental function altered?

11.5 Refining the model: A brain-specific knock-out of 11β-HSD2 during development

11.5.1 How to make a brain-specific 11β-HSD2 knock-out mouse

11.5.2 Do brain 11β-HSD2 knock-out mice display a ‘programmed affective phenotype’?

11.5.3 Future directions: A placenta-specific knock-out of 11β-HSD2

11.6 Perspectives

Cited references

Chapter 12 Early-Life Stress: Rodent Models, Lessons and Challenges

12.1 Why study early-life stress?

12.1.1 Early-life adversity is a major risk factor for psychopathology

12.1.2 The need for animal models of chronic early-life stress

12.2 Vulnerability of the developing brain

12.2.1 Maturation of the stress system

12.2.2 The stress hyporesponsive period

12.3 The mother is key: ELS models and manipulation of maternal input

12.3.1 Maternal separation

12.3.2 Manipulation of maternal care of a dam that remains with the pups

12.4 Validity and reliability of ELS models

12.4.1 The timing of stress manipulation

12.4.2 Genetics: species, strain and sex differences

12.4.3 The nature of the comparison group

12.5 Consequences of chronic early-life stress

12.5.1 Maternal separation

12.5.2 Limited nesting environment

12.6 Perspectives

Cited references

Further recommended reading Reviews of animal models of ELS

Key primary research papers using rodent ELS models

Additional related background and conceptual material

12.0.0 Set up pregnant females (dams)

12.0.0 Prepare limited nesting cages

12.0.0 Limited nesting manipulation

Chapter 13 Mothering Influences on Offspring Stress Response Mechanisms

13.1 Introduction

13.2 Maternal behaviour and care of the offspring

13.2.1 Rodents

13.2.2 Non-human primates

13.3 Impact of altered maternal care on infant stress responses: General considerations

13.3.1 Prolonged separation from mother

13.3.2 Brief separations from mother

13.3.3 Involvement of epigenetic mechanisms

13.4 Development of stress responsiveness in the offspring

13.4.1 Late fetal life

13.4.2 Neonatal life

13.5 Experimental preclinical models used for the study of maternal care and stress responses in off

13.5.1 Non-human primate models

13.5.2 Rodent models

13.6 Consequences of altered maternal care on offspring stress responses and behaviour

13.6.1 Non-human primates

13.6.2 Rodents

13.7 Potential mediating mechanisms

13.7.1 Offspring epigenetic modifications related to maternal care

13.7.2 Gene polymorphisms conferring vulnerability to stress-related pathologies

13.8 Conclusions

Cited references

Chapter 14 Translational Research in Stress Neuroendocrinology: 11β-HSD1, A Case Study

14.1 Introduction

14.1.1 The hypothalamic-pituitary-adrenal (HPA) axis

14.1.2 Dysregulation of the HPA axis and disease

14.1.3 Exposure to excess cortisol over the life course

14.1.4 Therapeutic manipulations

14.2 Small molecule drug discovery and development

14.2.1 Introduction

14.2.2 Target discovery

14.2.3 Hit identification

14.2.4 Lead optimization

14.3 11β-HSD1 inhibitors

14.3.1 Target and drug properties

14.3.2 Targeting the brain

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