Hormone - behavior relations of clinical importance: endocrine systems interacting with brain and behavior
Gespeichert in:
| Format: | Buch |
|---|---|
| Sprache: | English |
| Veröffentlicht: |
Amsterdam [u.a.]
Elsevier [u.a.]
2009
|
| Schlagworte: | |
| Online-Zugang: | Inhaltsverzeichnis |
| Beschreibung: | Includes bibliographical references and index |
| Beschreibung: | XXIX, 1152 S. Ill., graph. Darst. |
| ISBN: | 9780123749260 |
Internformat
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| 245 | 1 | 0 | |a Hormone - behavior relations of clinical importance |b endocrine systems interacting with brain and behavior |c ed. by Robert T. Rubin ... |
| 264 | 1 | |a Amsterdam [u.a.] |b Elsevier [u.a.] |c 2009 | |
| 300 | |a XXIX, 1152 S. |b Ill., graph. Darst. | ||
| 336 | |b txt |2 rdacontent | ||
| 337 | |b n |2 rdamedia | ||
| 338 | |b nc |2 rdacarrier | ||
| 500 | |a Includes bibliographical references and index | ||
| 650 | 4 | |a Human behavior |x Endocrine aspects | |
| 650 | 4 | |a Psychoneuroendocrinology | |
| 650 | 0 | 7 | |a Psychoendokrinologie |0 (DE-588)4122321-4 |2 gnd |9 rswk-swf |
| 650 | 0 | 7 | |a Psychopathologie |0 (DE-588)4047724-1 |2 gnd |9 rswk-swf |
| 653 | |a Psychoneuroendocrinology | ||
| 653 | |a Psychology, Pathological | ||
| 653 | |a Endocrine glands / Diseases | ||
| 653 | |a Molecular endocrinology | ||
| 653 | |a Human behavior / Endocrine aspects | ||
| 689 | 0 | 0 | |a Psychoendokrinologie |0 (DE-588)4122321-4 |D s |
| 689 | 0 | 1 | |a Psychopathologie |0 (DE-588)4047724-1 |D s |
| 689 | 0 | |5 DE-604 | |
| 700 | 1 | |a Rubin, Robert T. |e Sonstige |4 oth | |
| 856 | 4 | 2 | |m HBZ Datenaustausch |q application/pdf |u http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=018983557&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA |3 Inhaltsverzeichnis |
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Datensatz im Suchindex
| _version_ | 1804141157015355392 |
|---|---|
| adam_text | Titel: Hormone, behavior relations of clinical importance
Autor: Rubin, Robert T.
Jahr: 2009
Contents
Contributors xxv
About the Editors xxix
Principles of Translation^
Neuroendocrinology 1
R T Rubin and D W Pfaff
PART I
ENDOCRINE SYSTEMS INTERACTING
WITH BRAIN AND BEHAVIOR
CHAPTER 1
Genetic Transmission of Behavior and Its
Neuroendocrine Correlates 7
B Hambsch, R Landgraf, L Czibere, and C Touma
1.1 Introduction 8
1.2 Stress and the HPA System 8
1.2.1 Dysregulation of the Hypothalamic-
Pituitary-Adrenal Axis in Affective
Disorders 10
1.2.2 Animal Models Elucidating the
Molecular Basis of Neuroendocrine—
Behavior Interactions 11
1.2.2.1 Mice with targeted mutations
modulating HPA-axis function 11
1.2.2.2 Nontargeted genetic approaches 16
1-3 The Oxytocin and Vasopressin Systems 18
1.3.1 The Oxytocin System 19
1.3.1.1 Oxytocin 19
1.3.1.2 The oxytocin receptor 20
1.3.2 The Vasopressin System 21
1.3.2.1 Vasopressin 21
1.3.2.2 The vasopressin Via receptor 22
1.3.2.3 The vasopressin Vlb receptor 23
1.4 Tachykinins 24
1.4.1 Different Types of Tachykinins and
Receptors 24
1.4.2 Function of Tachykinin Signaling 25
1.5 Opioid Receptors 26
1.5.1 u-Opioid Receptors 27
1.5.1.1 ^-Opioid receptors in
nociception, stress response,
and post-traumatic stress
disorder 27
1.5.1.2 n-Opioid receptors in reward,
pleasure, and anxiety 28
1.5.1.3 Ji-Opioid receptor ligand
binding in different splice
variants 30
1.5.2 Endorphins 30
1.5.2.1 Maturation of the
P-endorphin-precursor
proopiomelanocortin 31
1.5.2.2 (5-Endorphin in motivation,
reward, and hedonic value 32
1.5.2.3 |3-Endorphin in stress, anxiety,
and post-traumatic stress
disorder 32
1.5.3 K-Opioid Receptors 33
1.5.3.1 K-Opioid receptors in reward
and aversion 33
1.5.3.2 K-Opioid receptors in
anxiety and ethanol-induced
anxiolysis 33
1.5.4 Dynorphins 34
1.5.4.1 Prodynorphin in analgesia,
reward, and aversion 34
1.5.5 S-Opioid receptors 35
1.5.5.1 8-Opioid receptors in
depression, anxiety, and
ethanol-induced anxiolysis 35 ¦
1.5.6 Enkephalins 36
1.5.6.1 Enkephalins in nociception and
anxiety 36
1.5.6.2 Enkephalins in stress-
induced anhedonia and
depression 37
1.6 Conclusion 37
References 38
vi Contents
CHAPTER 2
Hypothalamic-Pituitary-Adrenal Cortical
Axis 47
M E Rhodes, J M McKheen, D R Ripepi, and N E Gentile
2.1 Introduction 48
2.1.1 The Stress System 48
2.1.2 The HPA Axis 49
2.1.3 Corticotropin-Releasing Hormone 50
2.1.4 Arginine Vasopressin 52
2.1.5 Adrenocorticotropic Hormone 53
2.1.6 Glucocorticoids 54
2.2 Brain Regulation of Stress Responses 55
2.3 Physiological Responses to Stress 57
2.4 HPA Dysregulation: Conditions with
Altered HPA-Axis Activity 59
2.4.1 Hyperactive Conditions 59
2.4.2 Hypoactive Conditions 62
2.5 Conclusion 62
References 62
CHAPTER 3
Hypothalamic-Pituitary-Thyroid Axis 69
R TJoffe
3.1 Introduction 69
3.2 Hypothalamic-Pituitary-Thyroid Axis 70
3.3 Thyroid Disease 70
3.3.1 Hyperthyroidism 70
3.3.2 Hypothyroidism 71
3.3.3 Subclinical Hypothyroidism 71
3.3.4 Euthyroid Hypothyroxinemia 72
3.4 Major Psychiatric Disorders 72
3.4.1 Depression 72
3.4.1.1 Basal thyroid hormone levels 72
3.4.1.2 Use of thyroid hormones to
treat depression 74
3.4.2 Bipolar Disorder 76
3.4.2.1 Thyroid hormone levels 77
3.4.2.2 Effect of mood-stabilizing
treatments on thyroid hormone
levels 77
3.4.2.3 Use of thyroid hormones to
treat bipolar disorder 77
3.4.3 Other Psychiatric Disorders 78
3.4.3.1 Anxiety disorder 78
3.4.3.2 Schizophrenia 78
3.5 Conclusion 78
References 78
CHAPTER 4
Hypothalamic-Pituitary-Gonadal Axis in
Women 85
D R Rubittmv, P J Schmidt, S Meltzer-Brody, and V L Harsh
4.1 Introduction 86
4.2 Cell as Context 86
4.3 Developmental Stage as Context:
Critical Periods 87
4.4 Environment/Experience as Context 87
4.5 Reproductive Endocrine System 89
4.5.1 Hypothalamic—Pituitary—Ovarian Axis
and Gonadal Steroids 89
4.5.2 Dynamics of the Menstrual Cycle,
Menopause Transition, Pregnancy, and
Postpartum 89
4.5.2.1 Menstrual cycle 89
4.5.2.2 Menopause transition 90
4.5.2.3 Pregnancy and the postpartum 90
4.6 Reproductive Endocrine Systems and
the Pathophysiology of Mood Disorders 92
4.6.1 Neurotransmitters 92
4.6.2 Cell Signaling Pathways 93
4.6.3 Brain Regional Morphological Changes 93
4.6.4 The Hypothalamic—Pituitary—Adrenal
Axis 93
4.6.5 Role of Gonadal Steroids in
Modulating the Systems Involved in
Mood Disorders 94
4.6.5.1 Neuroregulation 94
4.6.5.2 Neural systems 94
4.6.5.3 Stress axis 95
4.7 Sexual Dimorphisms in Psychiatric
Disorders 96
4.7.1 Introduction 96
4.7.1.1 Depression 97
4.7.1.2 Physiological dimorphisms 97
4.8 Premenstrual Dysphoria 98
4.9 Hormonal Studies of PMD 98
4.9.1 Hypothalamic-Pituitary-Ovarian Axis 98
4.9.2 Context (Hormones as Triggers or
Treatments) 100
4.10 Perimenopausal Depression 101
4.11 Hormonal Studies of Perimenopausal
Depression 101
4.12 Gonadal Steroids as Treatments of
Mood Disorders 103
4.12.1 Estrogen Treatment 103
4.12.2 Dehydroepiandrosterone Treatment 104
4.13 Postpartum Psychiatric Disorders 104
4.14 Hormone Treatment Studies 105
4.14.1 Estrogen Treatment 105
4.14.2 Progesterone Treatment 106
4.15 Gonadal Triggers in Context 106
4.16 Context !07
References 107
CHAPTER 5
Hypothalamic-Pituitary-Gonadal Axis in
Men 119
R S Swerdloff C Wang, and A P Sinha Hikim
5.1 Hypothalamic Control 120
5.1.1 Hypothalamic Regulation
of Gonadotropin-Releasing
Hormone 120
5.1.2 GnRH Synthesis and Secretion 120
5.1.3 Origin and Migration of GnRH
Neurons during Development 121
5.2 Pituitary 121
5.2.1 Gonadotropin-Secreting Cells in the
Pituitary 121
5.2.2 Molecular Basis of Pituitary
Development 121
5.2.3 GnRH Receptors 121
5.2.4 Biochemistry of LH and FSH 122
5.2.5 LH and FSH Subunit Genes 122
5.2.6 Synthesis and Post-Translational
Processing of the Subunits 12 3
5.2.7 LH and FSH Receptor Structure 12 3
5.2.8 Clearance and Secretory Rhythms of
LH and FSH 123
5.2.9 Roles of LH and FSH in the Male 123
5.2.10 Gonadal Feedback Regulation of LH
and FSH 124
5.2.10.1 Gonadal steroids 124
5.2.10.2 Gonadal peptides (inhibin,
acrivins, and follistatins) and
feedback regulation of FSH 124
5.2.10.3 Summary 125
5.3 Testes-Leydig Cell Compartment 125
5.3.1 Testicular Steroidogenesis 125
5.3.2 T Transport and Metabolism 126
5.3.3 T Secretion during Fetal Development,
Childhood, Puberty, and Senescence 126
5.3.3.1 Fetal Leydig cell
steroidogenesis 126
5.3.3.2 Neonatal T secretion 127
5.3.3.3 Adrenarche and puberty 127
5.3.3.4 Male senescence: Decreased T
and other anabolic hormones 129
5.3.4 T as a Hormone, Prehormone, and
Paracrine Factor 130
5.3.5 Androgen Receptor 131
5.3.5.1 AR gene, protein structure, and
regulatory proteins 131
5.3.5.2 AR defects 132
5.3.6 T Target Organs 132
5.3.7 Role of T in Normal Sexual Function
and Erectile Physiology 132
Contents vii
5.3.8 T Deficiency. Male Hypogonadism 134
5.3.8.1 Etiologies 134
5.3.8.2 Clinical manifestations of
hypogonadism: Clinical history
and physical examination 136
5.3.8.3 Laboratory tests in assessment
of hypogonadism 13 7
5.3.8.4 Treatment of androgen
deficiency 137
5.4 Spermatogenesis and Sperm Transport 138
5.4.1 Hormonal Regulation of
Spermatogenesis 139
5.4.1.1 Gonadotropins and androgen
regulation of spermatogenesis 139
5.4.1.2 Gonadotropins and androgen
regulation of programmed
germ cell death 141
5.4.1.3 Gonadotropins and androgens
as germ cell survival factors 142
5.4.1.4 Sertoti cell control of
spermatogenesis 143
5.4.2 Sperm Transport 144
5.4.3 Environmental Agents and the
Reproductive System 144
5.4.4 Male Infertility 144
5.4.4.1 Prevalence and incidence 144
5.4.4.2 Etiology 144
5.4.4.3 Approach to the diagnosis of
male infertility 144
5.4.4.4 Management of male infertility 145
5.5 Sexual Dysfunction 145
5.5.1 Decreased Libido 145
5.5.2 Ejaculatory Failure and Impaired Orgasm 146
5.5.3 Erectile Dysfunction 146
5.5.3.1 Prevalence 146
5.5.3.2 Etiology 146
5.5.3.3 Clinical management of ED 146
References 146
Further Reading 155
CHAPTKR6
Sex Differences in Human Brain Structure
and Function 157
/, Cabill
6.1 Introduction 157
6.2 Are Sex Influences in the Human Brain
Small and Unreliable? 157
6.3 Sex Influences on Human Brain
Function Generally Considered 158
6.4 Sex Differences in Emotional Memory 160
6.5 Amygdala Activity and Emotional
Memory in Humans - Emergence of
Sex Effects 160
viii Contents
6.6 Sex-Related Hemispheric
Lateralization of the Amygdala
Relationship to Emotional Memory 160
6.7 Sex Difference in Human Amygdala
Functional Connectivity at Rest 161
6.8 Relationship of the Sex-Related
Amygdala Hemispheric Specialization
to Hemispheric Global/Local
Processing Bias 162
6.8.1 Other Influences of Sex on Neural and
Hormonal Mechanisms of Emotional
Memory 162
6.9 Summary 164
References 164
Further Reading 165
CHAPTER 7
Sex Differences in CNS Neurotransmitter
Influences on Behavior 167
M E Rhodes, TJ Cnel, and A N Nord
7.1 Introduction 168
7.1.1 Sexual Dimorphism of the Mammalian
CNS 171
7.1.2 Sexual Diergism - Physiological
Differences between the Sexes 171
7.2 Acetylcholine 172
7.2.1 Cholinergic Nervous System 172
7.2.2 Sexual Diergism in Choline, Choline
Transport, and Acetylcholine 172
7.2.3 Sexual Diergism in Cholinergic
Enzymes 173
7.2.4 Sexual Diergism in Cholinergic
Receptor Activity 174
7.2.5 Influence of Gonadal Steroids on
Cholinergic Systems 175
7.2.6 Cholinergic Sexual Diergism in
Relation to Learning, Memory, and
Other Behaviors 176
7.2.7 Acetylcholine and the HPA axis 176
7.2.7.1 Sexual diergism in basal HPA-
axis activity 177
7.2.7.2 Influence of gonadal steroids
on HPA-axis activity 177
7.2.7.3 Sexual diergism of HPA-axis
responses to stimulation 177
7.2.7.4 Sexual diergism of HPA-axis
responses to cholinergic
stimulation and antagonism 179
7.3 Dopamine 182
7.3.1 Dopaminergic Age-Related Sex
Differences 182
7.3.2 Sexual Diergism, Gonadal Hormones,
and Dopamine 182
7.4 Gamma-Aminobutyric acid 183
7.4.1 Sex Differences in GABAergic Systems 183
7.4.2 Influence of Gonadal Steroids on
GABAergic Sex Differences 184
7.4.3 Sexual Diergism in GABAergic
Systems 185
7.5 Norepinephrine 186
7.5.1 Sexual Dimorphism and Diergism of
Noradrenergic Systems 186
7.6 Serotonin 188
7.6.1 Sexual Dimorphism and Diergism of
Serotonergic Systems 188
7.7 Vasopressin 189
7.7.1 Sexual Dimorphism of AVP 189
7.7.2 Sexual Diergism of AVP 190
7.7.3 Influence of Gonadal Steroids on AVP
Secretion 191
7.8 Implications and Relevance of Sexual
Diergism 192
7.8.1 Behavioral Relevance of Sexual
Diergism 193
7.8.2 Sexual Diergism in Relationship to
Disease 194
7.8.3 Therapeutic Implications of Sexual
Diergism 194
7.9 Conclusion 195
References 196
CHAPTER 8
Gonadal Hormones and Sexual
Differentiation of Human Brain and Behavior 207
M Hines
8.1 Introduction 208
8.2 Definitions and Theoretical Models 208
8.2.1 Definitions 208
8.2.1.1 Organization and activation 208
8.2.1.2 Sex differences and gender
differences 209
8.2.2 Theoretical Models 209
8.2.2.1 The classic model 209
8.2.2.2 The gradient model 210
8.2.2.3 Active feminization 210
8.2.2.4 Complexity and multiple
models 210
8.2.3 Summary 211
8.3 Hormonal Influences on Human
Sexual Differentiation: Sources of
Information 211
8.3.1 Syndromes Involving Prenatal
Hormonal Abnormality 212
8.3.1.1 Congenital adrenal hyperplasia 212
8.3.1.2 Androgen insensitivity
syndrome 213
8.3.1.3 Androgen biosynthesis
deficiencies (5-aR and 17-HSD
deficiencies) 213
8.3.1.4 Hypogonadotropic
hypogonadism 213
8.3.1.5 Turner syndrome 213
8.3.1.6 Cloacal exstrophy 214
8.3.1.7 Penile agenesis (aphallia) 214
8.3.1.8 Ablatio penis 214
8.3.2 Hormone Administration during
Pregnancy 214
8.3.3 Normal Variability in Hormones 215
8.4 Hormonal Influences on Human Sexual
Differentiation: Human Behavioral Sex
Differences 216
8.4.1 Core Gender Identity 216
8.4.2 Sexual Orientation 217
8.4.3 Gender-Role Behavior 217
8.4.3.1 Childhood play 217
8.4.3.2 Cognitive abilities 217
8.4.3.3 Emotion, temperament, and
personality 219
8.4.3.4 Psychopathology 219
8.4.3.5 Neural asymmetries 219
8.5 Hormones and Sexual Differentiation
of Human Behavior: Findings 220
8.5.1 Core Gender Identity 220
8.5.2 Sexual Orientation 222
8.5.3 Childhood Play 224
8.5.4 Cognition 226
8.5.4.1 General intelligence 226
8.5.4.2 Specific cognitive abilities 227
8.5.5 Emotion, Temperament, and
Personality 230
8.5.5.1 Aggression 230
8.5.5.2 Empathy 231
8.5.5.3 Interest in parenting 231
8.5.5.4 Other personality
characteristics 231
8.5.6 Psychopathology 231
8.5.7 Neural Asymmetries 232
8.5.7.1 Hand preferences 232
8.5.7.2 Language lateralization 233
8.6 Hormonal Influences on Neural Sexual
Differentiation 233
8.6.1 Sex Differences in Neural Structure
and Function 233
8.6.1.1 Brain size 233
8.6.1.2 Anterior hypothalamic/
preoptic area 233
8.6.1.3 The bed nucleus of the stria
terminals 234
8.6.1.4 The anterior commissure 234
8.6.1.5 The suprachiasmatic nucleus 234
Contents ix
8.6.1.6 The corpus callosum 235
8.6.1.7 The cerebral cortex 236
8.6.2 Hormones and the Human Brain 237
8.7 Summary and Conclusions 237
8.7.1 Fitting a Theoretical Model 238
8.7.2 Mechanisms of Hormone Action 238
8.7.3 Clinical and Theoretical Importance 239
References 239
CHAPTER 9
Human Puberty: Physiology and Genetic
Regulation 249
B A Kaminski and M R Palmert
9.1 Introduction 249
9.2 Prepubertal Development 250
9.2.1 Prenatal and Postnatal Development 250
9.2.2 The Juvenile Pause 250
9.2.3 Ontogeny of Gonadotropin Secretion 250
9.3 Physical Changes of Puberty 251
9.3.1 Bone Age 252
9.4 Timing of Pubertal Onset 252
9.5 Genetic Basis of Pubertal Timing 253
9.5.1 Approaches to Identifying Genetic
Factors 253
9.5.2 Insights from Single Gene Disorders 255
9.5.2.1 Idiopathic hypogonadotropic
hypogonadism 255
9.5.2.2 Kallmann syndrome 256
9.5.2.3 Leptin and other genes 256
9.5.3 Genetic Variation in Normal Puberty 257
9.5.4 Quantitative Trait Loci Associated with
Timing of Puberty 258
9.6 Neuroendocrine Regulation of
Pubertal Onset 260
9.7 Environmental Influences on Pubertal
Timing 260
9.7.1 Obesity and the Relationship to
Pubertal Timing 260
9 7 2 Kndocrine Disrupters and
F.nvironmental Influences 261
9.8 Behavior Related to Variations in
Pubertal Timing 261
9 8.1 Psychosocial Changes of Puberty 261
9.8.2 Brain Development during Puberty 262
9.9 Conclusion 263
References 263
CHAPTER 10
The Biology of Sexual Orientation and
Gender Identity 271
FJ Sandxz, S Bocklandl, and E Vilain
x Contents
10.1 Introduction 272
10.2 Sexual Orientation 272
10.2.1 Defining and Describing
Homosexuality 272
10.2.2 Theory 273
10.2.3 The Biology of Sexual Orientation 273
10.2.3.1 Hormonal influences 273
10.2.3.2 Correlational studies 274
10.2.3.3 Genetics studies 277
10.3 Gender Identity 278
10.3.1 Defining and Describing
Transsexualism 278
10.3.1.1 Gender identity disorder 279
10.3.1.2 Transgender 279
10.3.1.3 Transsexualism 279
10.3.1.4 Primary and secondary MtF
transsexuals 280
10.3.2 Theory 280
10.3.3 The Biology of Gender Identity 281
10.3.3.1 Hormonal influences 281
10.3.3.2 Correlational studies 281
10.3.3.3 Genetic studies 283
10.4 Conclusion 284
References 284
Further Reading 289
CHAPTER 11
Sexual Orientation in Men and Women 291
L jf Gooren and W Byne
11.1 History of the Concept of
Homosexuality 291
11.1.1 The Third Sex as Homosexuality 292
11.1.2 Hirschfeld and the Concept of the
Third Sex 292
11.1.3 The Hormonal Theories of Steinach 292
11.2 Paradigm of Biomedical Research into
Homosexuality 293
11.3 The Search for Cross-Sex Endocrine
Findings in Homosexuals 295
11.4 The Prenatal Hormonal Hypothesis 296
11.4.1 Prenatal/Postnatal Testosterone
Physiology 296
11.4.2 Impact of Prenatal Hormones on
Sexual Orientation/Gender Identity:
Lessons from Clinical Syndromes 297
11.4.3 Disorders of Sexual Differentiation 298
11.4.3.1 Complete androgen
insensitivity 298
11.4.3.2 Partial androgen resistance
syndromes 299
11.4.3.3 5a-Reductase deficiency 299
11.4.3.4 17P-Hydroxysteroid
dehydrogenase defiency 300
11.4.3.5 Congenital adrenal (virilizing)
hyperplasia in women 300
11.4.3.6 Cloacal exstrophy 301
11.4.3.7 Summary of the findings in
subjects with disorders of
sexual differentiation 302
11.5 Digit Ratios as Marker of Prenatal
Testosterone 302
11.6 The Fraternal Birth Order in Males 303
11.7 Hormonal Effects on the Developing
Brain 304
11.7.1 Nucleus Intermedius 304
11.7.2 The Caudal Part of the Bed Nucleus of
the Stria Terminalis 305
11.7.3 Interstitial Nucleus of the Anterior
Hypothalamus 3 305
11.7.4 Other Neuroanatomical Studies 306
11.8 Conclusion 306
References 307
CHAPTER 12
Sex Differences in Competitive Confrontation
and Risk-taking 311
M Wilson, M Daly, and N Pound
12.1 Introduction 311
12.2 An Evolutionary Psychological
Perspective 312
12.2.1 Decision-Making Adaptations 313
12.2.2 Adaptation versus Pathology 314
12.2.3 Sexual Selection and Competition 315
12.2.4 Homicide as an Assay of Competitive
Confrontation and Risk Taking 316
12.2.5 The Sex Difference in Human
Intrasexual Competition and Violence 317
12.2.6 Demography of Masculine Competitive
and Risk-Taking Inclinations 318
12.2.7 Discounting the Future 321
12.2.8 Inequity and Lethal Competitive
Violence 323
12.2.9 Making Sense of Individual Differences 325
12.2.10 Testosterone and the Modulation of
Confrontational Competitive Risk
Taking 327
12.2.11 Testosterone as a Mediator of Mating
Effort 328
12.2.12 Testosterone s Costs and Honest
Signaling 330
12.3 Concluding Remarks 332
References 333
Further Reading 338
CHAPTER 13
Prolactin Actions in the Brain 339
D R Qrattan and R S Bridges
13.1 Introduction 340
13.2 Hypothalamic Control of PRL
Secretion 340
13.2.1 PRL Secretion Is Inhibited
by Dopamine from the
Hypothalamus 340
13.2.2 Short-Loop Negative Feedback 341
13.2.3 Role of a PRL-Releasing Factor 344
13.3 Access of PRL to the Brain 344
13.3.1 Transport into the Central Nervous
System 344
13.3.2 The Brain Also Produces PRL 345
13.4 PRL Receptor Expression in the Brain 345
13.4.1 High Levels of Expression of PRL
Receptors in the Choroid Plexus 345
13.4.2 PRL Receptors Are Widespread in the
Hypothalamus 346
13.4.3 Regulation of PRL Receptor
Expression in the Brain 348
13.5 Changes in Patterns of PRL Secretion 349
13.5.1 Estrous/Menstrual Cycle 349
13.5.2 Stress-Induced Changes in PRL
Secretion 349
13.5.3 Pregnancy 350
13.5.4 Suckling-Induced Release of PRL 351
13.5.5 Mechanisms Contributing to the
Change in the Neuroendocrine Control
of PRL Secretion during Late
Pregnancy and Lactation 351
13.5.5.1 Change in PRL signal
transduction in TIDA neurons 351
13.5.5.2 Role of ovarian steroids in the
regulation of PRL feedback
during pregnancy and lactation 352
13.5.5.3 A proposed model for the
pregnancy-induced adaptation
of the neuroendocrine control
of PRL secretion 353
13.6 Brain Actions of PRL in Mammals 354
13.6.1 Maternal Behavior 354
13.6.2 Stress Response and Anxiety 356
13.6.3 Regulation of Oxytocin Neurons 356
13.6.4 Regulation of Reproductive Behavior
and Fertility 357
13.6.5 Neurorrophic Effects, Neurogenesis,
and Glial Cell Function 358
13.6.6 Appetite and Food Intake 358
13.6.7 PRL and the Neurobiological
Adaptation to Pregnancy and Lactation 359
Contents xi
13.7 Conclusion 360
References 360
CHAPTKR 14
Growth Hormone and Insulin-Like Growth
Factor-I: Effects on the Brain 373
Z I.aron
14.1 Introduction 374
14.2 The GHRH-GH-IGF-I Axis 374
W.2.1 Growth Hormone-Releasing Hormone 374
14.2.2 Human GURU Receptor 374
14.2.3 Gil Secretary s 374
14.2.4 Ghrelin 375
14.2.5 Somatostatin 375
14.2.6 Somatostatin Receptors 375
14.2.7 Cortistatin 375
14.2.8 Human Gil 375
14.2. » GH Receptor 375
14.2.10 Gil-Binding Protein 375
14.2.11 Insulin-Like Growth Factor I 375
14.2.12 IGI -Bindinn Proteins 376
14.2.H IGF-I Receptor 376
14.3 GH Crosses the Blood-Brain Barrier 376
14.4 IGF-1 Crosses the BBB 377
14.5 Expression of GH in the Central
Nervous Tissue 377
14.6 Expression of IGF-I and Its Receptor
Gene in the Nervous Tissue 378
14.7 IGFBPs in the Brain 378
14.8 IGF as a Neurotropic and
Antiapoptotic Factor 379
14.9 GH/IGF-I and Cerebral Myelinization 380
14.10 Effect of GH and IGF-I on Brain
Development and Growth - Animal
Studies 380
14.11 Additional Effects of IGF-I on the
Central and Peripheral Nervous System 380
14.12 GH and IGF-I Effects on Brain Growth
in Children 381
14.13 Effect of GH and/or IGF-I on
Intellectual Performance 381
14.14 Influence of Untreated and Treated GH
and IGF-I Deficiency on Psychosocial
Well-Being and Quality of Life 383
14.15 GH and IGF-I and the Aging Brain 384
14.16 GH and IGF-I Effects on Memory in
mice 384
xii Contents
14.17 GH and IGF-I in Neurological
Disorders 385
14.18 GH and IGF-I in Psychiatric Disorders 385
14.19 Psychological Effects of GH
Administration to Nongrowth
Hormone-Deficient Short Children 385
14.20 GH and IGF-I and Risk for Brain
Malignancy 386
14.21 Conclusions 386
References 386
Further Reading 394
CHAPTER 15
Neurosteroids: From Basic Research to
Clinical Perspectives 395
CAFrye
15.1 Introduction 396
15.2 The Brain is an Endocrine Organ -
Neurosteroidogenesis 396
15.2.1 The Discovery of Biosynthesis 397
15.2.2 Peripheral-Type Benzodiazepine
Receptor Recognition Site 397
15.2.3 Metabolic Pathways 397
15.2.4 Metabolic Enzymes 397
15.2.5 Patterns in Secretion 399
15.3 Actions of Neurosteroids 399
15.3.1 Nonclassical Actions of Neurosteroids 399
15.3.2 Actions of Neurosteroids through
GABAA Receptors 399
15.3.3 Other Targets for Neurosteroids 400
15.4 Neurosteroids Clinical Relevance 400
15.4.1 Neurosteroids and Neuronal Growth
and Development 400
15.4.2 Neurosteroids and Gestation 400
15.4.3 Neurosteroids and Preterm Birth 401
15.4.4 Neurosteroids and Autism Spectrum
Disorders 401
15.4.5 Neurosteroids and Drug Abuse 401
15.4.5.1 Neurosteroids and alcohol 401
15.4.5.2 Neurosteroids and cocaine 402
15.4.6 Neurosteroids and Depression 402
15.4.6.1 Neurosteroids and depression
- etiology 402
15.4.6.2 Neurosteroids and depression
— treatment 403
15.4.7 Neurosteroids and Anxiety 403
15.4.8 Neurosteroids and Mood
Dysregulation 403
15.4.9 Neurosteroids and Schizophrenia 404
15.4.10 Neurosteroids, Aging, Menopause, and
Hormone Therapy 404
15.4.11 Neurosteroids and Neurodegeneration 405
15.4.11.1 Neurosteroids and seizure
disorder 405
15.4.11.2 Neurosteroids and AD 405
15.4.11.3 Neurosteroids and
Niemann-Pick type C 406
15.4.12 Neurosteroids, Apoptosis, and
Neurogenesis 406
15.5 Conclusions 407
References 407
Further Reading 414
CHAPTER 16
Brain Peptides: From Laboratory to Clinic 417
T D Geracioti, Jr., J R Stra-wn, N N Ekbator, M Wortman,
andJKaskmi) 417
16.1 Introduction 418
16.2 Growth-Hormone-Releasing Hormone 419
16.2.1 Regulation of GHRH 419
16.2.2 Functions of GHRH 419
16.2.3 Growth Hormone 420
16.2.4 Clinical Implications: Disease States
with GHRH-Related Abnormalities 421
16.2.5 Clinical Implications: Therapeutics 421
16.3 Gonadotropin-Releasing Hormone 422
16.3.1 GnRH Regulation 422
16.3.2 Functions of GnRH 422
16.3.3 Clinical Implications 423
16.4 Somatostarin 424
16.4.1 Localization 424
16.4.2 Somatostarin Receptors 425
16.4.3 Physiologic Effects 425
16.4.4 Clinical Implications 425
16.5 Corticotropin-Releasing Hormone 425
16.5.1 CRH Regulation 426
16.5.2 CNS CRH Circadian Rhythm 426
16.5.3 The CRH Receptor 426
16.5.4 Physiologic Effects 427
16.5.5 Clinical Implications 427
16.6 Thyrotropin-Releasing Hormone 429
16.6.1 Regulation of TRH 429
16.6.2 TRH Receptors 429
16.6.3 TRH Function 429
16.6.4 Clinical Implications 430
16.7 POMC-Derived Neuropeptides:
Melanocortins 431
16.7.1 Tissue-Specific Processing of POMC 431
16.7.2 Melanocyte-Stimulating Hormone 431
16.7.3 Lipotropin 432
16.7.4 Distribution of POMC and Its Derived
Peptides 432
16.7.5 Regulation of the POMC Gene and
POMC-Derived Peptides 432
16.7.6 Melanocortin Receptors and Second
Messengers 432
16.7.7 Functions of ACTH and MSH 432
16.7.8 Other Effects of Melanocortins 433
16.7.9 Clinical Implications 433
16.8 Opioid Peptides 435
16.8.1 Prodynorphin (Proenkephalin B) and
Dynorphin 435
16.8.2 Proenkephalin A 435
16.8.3 Nociceptin 435
16.8.4 Endomorphin 435
16.8.5 Opiate-Receptor Distribution 436
16.8.6 Role of Receptor Subtypes 436
16.8.7 Physiologic Roles of Opioids 436
16.8.8 Clinical Implications 437
16.9 Oxytocin 438
16.9.1 Processing and Metabolism of
Oxytocin 438
16.9.2 Regulation of the Oxytocin Gene and
Peptide 439
16.9.3 Oxytocin Receptors 439
16.9.4 Behavioral Effects of Oxytocin 440
16.9.5 Clinical Implications 440
16.10 Vasopressin 441
16.10.1 AVP Precursor and Post-Translational
Products 441
16.10.2 AVP Receptors 441
16.10.3 Physiologic Functions 441
16.10.4 Behavioral Effects 442
16.10.5 Clinical Implications of VP 442
16.11 Cholecystokinin 443
16.11.1 Structure of CCK 443
16.11.2 Localization 443
16.11.3 CCK Receptors 444
16.11.4 CCK Physiology 444
16.11.5 Clinical Implications 445
16.12 Neuropeptides of Emerging or
Expanding Psychiatric Interest 446
16.12.1 Substance P 446
16.12.2 Clinical Implications: Populations of
Interest 446
16.12.3 Clinical Implications: Diagnostic
Testing 44
16.12.4 Clinical Implications: Therapeutics 446
16.12.5 Neuropeptide Y 447
16.12.6 Clinical Implications: Populations of
Interest 44?
16.12.7 Clinical Implications: Therapeutics 448
16.12.8 Orexins (Hypocretins) 448
16.12.9 Clinical Implications: Special
Populations 449
16.12.10 Clinical Implications: Diagnostics 449
16.12.11 Clinical Implications: Therapeutics 449
Contents xiii
16.13 Concluding Remark 449
References 449
Further Reading 461
CHAPTER 17
Melatonin Actions in the Brain 465
A J Lewy, J Emens, J Songer, and J Rough
17.1 Hormones 465
17.2 Melatonin as a Neurohormone 466
17.3 Circadian Physiology 467
17.4 Melatonin as a Phase Marker 470
17.5 Circadian Time 471
17.6 Zeitgeber Time 471
17.7 Effects of Light on Circadian Rhythms 471
17.8 Effects of Melatonin on Circadian
Rhythms 472
17.9 Soporific Effects of Melatonin 472
17.10 Safety of Melatonin 473
17.11 Abnormalities in Circadian Rhythms 473
17.11.1 Blindness 473
17.11.2 Advanced and Delayed Sleep Phase
Syndromes 474
17.11.3 Jet Lag 475
17.11.4 Shiftwork 476
17.11.5 Seasonal Affective Disorder (Winter
Depression) 476
17.12 Speculation on the Function of
Endogenous Melatonin Production 480
17.13 A Possible Bioassay for Sensitivity to
the Weak Zeitgebers Reveals a Gender
Difference 480
17.14 Summary 481
References 481
Further Reading 486
CHAPTER 18
Neuroendocrine-Immune Interactions:
Implications for Health and Behavior 487
T W W Pace, C I. Raism, and A H Miller
18.1 Overview of the Immune System 488
18.1.1 Innate versus Acquired Immunity 489
18.1.2 Immune System Tests 491
18.1.3 Regulation of the Immune Response 492
18.2 Foundations of Neuroendocrine-
Immune Interactions 492
18.3 Neuroendocrine Factors in Immune
Regulation 494
18.3.1 Glucocorticoids 494
18.3.2 Catecholamines 495
xiv Contents
18.3.3 Corticotropin-Releasing Hormone 496
18.3.4 Other Factors 497
18.4 Role of Cytokines in the Regulation of
the Neuroendocrine System and
Behavior 498
18.4.1 Pathways of Immune to Brain Signaling 498
18.4.2 Cytokine Network in the Brain 498
18.4.3 Impact of Cytokines on Nervous and
Endocrine System Function 499
18.4.3.1 Cytokine effects on the HPA
axis 499
18.4.3.2 Cytokine effects on
glucocorticoid receptors 499
18.4.3.3 Behavioral effects of cytokines 502
18.5 The Impact of Stress on the Immune
System 503
18.5.1 Acute Stress 503
18.5.2 Chronic Stress 507
18.5.3 Psychosocial Variables Mediating
Neuroendocrine—Immune Interactions
during Stress 508
18.6 Neuroendocrine—Immune Interactions
in Depression 509
18.6.1 Major Depression and Immune
Parameters 509
18.6.2 Depression and Immune Activation 510
18.7 Model for Neuroendocrine-Immune
Interactions in Clinical Disease 512
18.7.1 A Neuroendocrine Diathesis Model of
Inflammation 512
18.8 Therapeutic Implications of
Neuroendocrine—Immune Interactions 514
18.8.1 Behavioral Interventions in
Immunologic Disorders 514
18.8.2 Neuroendocrine Interventions in
Immunologic Disorders 515
18.8.3 Immune Interventions in Behavioral
Disorders 515
References 516
PART II
ENDOCRINOLOGICALLY IMPORTANT
BEHAVIORAL SYNDROMES
CHAPTER 19
Diseases of Hypothalamic Origin 525
J D Carmichael and G D Bmunstein
19.1 Anatomy 526
19.2 Hypothalamic Functions 526
19.2.1 Water Metabolism 527
19.2.2 Temperature Regulation 528
19.2.3 Appetite Control 530
19.2.4 Sleep-Wake Cycle and Orcadian
Rhythm Control 530
19.2.5 Regulation of Visceral (Autonomic)
Function 531
19.2.6 Emotional Expression and Behavior 531
19.2.7 Memory 531
19.2.8 Control of Anterior Pituitary Function 531
19.3 Pathophysiological Principles 532
19.4 Manifestations of Hypothalamic
Disease 533
19.4.1 Disorders of Water Metabolism 533
19.4.1.1 Central diabetes insipidus 533
19.4.1.2 Adipsic or essential
hypernatremia 535
19.4.1.3 Syndrome of inappropriate
secretion of antidiuretic
hormone 536
19.4.1.4 Cerebral salt wasting 537
19.4.1.5 Reset osmostat 537
19.4.2 Dysthermia 537
19.4.2.1 Hyperthermia 537
19.4.2.2 Hypothermia 538
19.4.2.3 Poikilothermia 539
19.4.3 Disorders of Caloric Balance 539
19.4.3.1 Hypothalamic obesity 539
19.4.3.2 Hypothalamic cachexia in
adults 539
19.4.3.3 Diencephalic syndrome of
infancy 539
19.4.3.4 Anorexia nervosa 540
19.4.3.5 Diencephalic glycosuria 541
19.4.4 Sleep—Wake Cycle Circadian
Abnormalities 541
19.4.5 Behavioral Abnormalities 541
19.4.6 Diencephalic Epilepsy 542
19.5 Disordered Control of Anterior
Pituitary Function 542
19.5.1 Hyperfunction Syndromes 542
19.5.1.1 Precocious puberty 542
19.5.1.2 Acromegaly 543
19.5.1.3 Cushing s disease 544
19.5.1.4 Hyperprolactinemia 544
19.5.2 Hypofunction Syndromes 544
19.5.2.1 Acquired hypogonadotropic
hypogonadism 544
19.5.2.2 Congenital GnRH deficiency
(idiopathic hypogonadotropic
hypogonadism) 545
19.5.2.3 Growth hormone deficiency 545
19.5.2.4 Hypothalamic hypoadrenalism 546
19.5.2.5 Hypothalamic hypothyroidism 546
19.6 Specific Hypothalamic Disorders 547
19.6.1 Prader-Willi Syndrome 547
19.6.2 Septo-Optic Dysplasia 548
19.6.3 Psychosocial Short Stature 548
19.6.4 Pseudocyesis 550
19.7 Neoplasms Involving the
Hypothalamus 550
19.7.1 Hypothalamic Hamartoma 550
19.7.2 Germ Cell Tumor 551
19.7.3 Optic Chiasm and Hypothalamic
Glioma 553
19.7.4 Craniopharyngioma 553
19.7.5 Suprasellar Meningioma 554
19.7.6 Suprasellar Arachnoid Cyst 554
19.7.7 Colloid Cyst of the Third Ventricle 555
19.8 Infiltrative Disorders 555
19.8.1 Neurosarcoidosis 555
19.8.2 Histiocytosis 555
19.8.3 Leukemia 556
19.8.4 Paraneoplastic Syndrome 556
19.9 Cranial Irradiation 556
19.10 Traumatic Brain Injury 557
19.11 Critical Illness 558
References 558
CHAPTER 20
Stress and Anxiety Disorders 569
£ A Young, S N Garfinkel, and I Liberzon
20.1 Introduction 569
20.1.1 Stress, Fear, and Anxiety 569
20.1.2 Anxiety Disorders and Stressful Events -
Is There a Connection? The Role of
Life Events 570
20.2 Description of Basic Stress and Anxiety
Systems 571
20.2.1 Stress-Response Systems: Stress and
HPA-Axis Regulation 571
20,2.1.1 Links between HPA axis and
noradrenergic function in
animal studies 571
20.2.2 Anxiety and Fear - Neural Pathways 572
20.2.3 The HPA Axis in Panic Disorder and
Other Anxiety Disorders 574
20.2.4 The HPA Axis in PTSD 574
20.4 The Sympthetic Nervous System in
Anxiety Disorders 577
20.4.1 Central Noradrenergic Regulation in
Anxiety Disorders 577
20.4.2 Other Noradrenergic Markers in Panic
Disorders 577
20.4.3 Peripheral Sympathetic Nervous
System Function in PTSD 578
20.5 Modeling Stress/Anxiety Interaction in
Animals 579
20.5.1 Modeling Fear versus Modeling
Abnormal Anxiety 579
Contents xv
20.5.2 Behavioral Test versus Models of
Anxiety Disorders 579
20.5.3 Effects of Stressful Exposure on
Endocrine and Behavioral Variables 580
20.5.3.1 Stressor characteristics 580
20.5.4 Summary of Animal Models 581
20.6 Imaging the Fear and Anxiety Pathways 581
20.6.1 Structural Neuroimaging in PTSD and
Anxiety Disorders - Is Cortisol Bad for
Your Hippocampus? 581
20.6.2 Functional Imaging of Stress/Anxiety
States 582
20.6.2.1 Imaging of fear in normal
controls 582
20.6.2.2 Functional neuroimaging in
anxiety disorders 583
20.6.2.3 Functional neuroimaging in
PTSD 584
References 586
Further Reading 591
OHAPTKR 21
Mood Disorders 593
R T Rubin and H J Carroll
21.1 Introduction 595
21.1.1 Classification 595
21.1.2 Diagnostic Criteria and Depressive
Subtypes 595
21.1.3 Genetics 596
21.1.4 Epidemiology 596
21.1.5 Neurocircuitry of Depression 596
21.1.6 Neurotransmitter and Neuromodulator
Function 597
21.1.6.1 Acetylcholine and
norepinephrine 597
21.1.6.2 Serotonin 598
21.1.6.3 Dopamine 598
21.1.6.4 Other neuroendocrine peptides 598
21.1.6.5 Brain-derived neurotrophic
factor 599
21.1.6.6 Neurosteroids and neuroactive
steroids 599
21.2 Hypothalamic-Pituitary-
Adrenocortical Axis 599
21.2.1 Secretion of Adrenocorticotropic
Hormone and Cortisol in Depression 599
21.2.2 Secretion of Corticotropin-Releasing
Hormone in Depression 601
21.2.3 Secretion of Arginine Vasopressin in
Depression 601
21.2.4 Perturbation Tests of HPA-Axis
Function in Depression 602
21.2.4.1 Dexamethasone suppression
test 602
21.2.4.2 CRH stimulation test 603
xvi Contents
21.2.4.3 ACTH stimulation test 603
21.2.4.4 Serotonergic stimulation 603
21.2.5 Pituitary and Adrenal Volumetric
Studies in Depression 604
21.2.5.1 Pituitary gland 604
21.2.5.2 Adrenal gland 604
21.2.6 Glucocorticoid Receptor Function in
Depression 604
21.2.7 Effects of Antidepressants on the HPA
Axis 605
21.2.8 CRH-Receptor Antagonists in the
Treatment of Depression 605
21.2.9 Cortisol Synthesis Inhibitors and
Glucocorticoid Receptor Antagonists
in the Treatment of Depression 605
21.3 Hypothalamic-Pituitary-Thyroid Axis 606
21.3.1 Basal Thyroid Function in Depression 606
21.3.2 TRH Stimulation of TSH in
Depression 606
21.3.3 Relationship to the HPA Axis 606
21.3.4 Diagnostic and Prognostic Utility of the
TRH Stimulation Test 607
21.3.5 Adjuvant Therapy with Thyroid
Hormones 607
21.3.5.1 Acceleration of antidepressant
effect 607
21.3.5.2 Augmentation of antidepressant
effect 607
21.3.5.3 Mode of action of thyroid
hormone augmentation 607
21.4 Growth Hormone (Somatotropin) 608
21.4.1 Regulation of GH Secretion 608
21.4.2 Basal GH Secretion in Depression 608
21.4.3 Monoamines and GH Secretion in
Depression 608
21.4.3.1 Norepinephrine 608
21.4.3.2 Dopamine 609
21.4.3.3 Serotonin 609
21.4.3.4 Acetykholine 609
21.4.3.5 Gamma-aminobutyric acid 609
21.4.4 Glucocorticoids and GH Secretion in
Depression 609
21.4.5 Peptide-Stimulated GH Secretion in
Depression 609
21.4.5.1 Growth hormone-releasing
hormone 609
21.4.5.2 Corticotropin-releasing
hormone 610
21.4.5.3 Thyrotropin-releasing
hormone 610
21.5 Hypothalamic—Pituitary-Gonadal Axis 610
21.5.1 Depressed Men 610
21.5.2 Premenopausal Depressed Women 610
21.5.3 Peri/Postmenopausal Depressed Women 610
21.5.4 Gonadal Steroid Pharmacotherapy 611
21.6 Prolactin 611
21.6.1 Basal Prolactin Secretion in Depression 611
21.6.2 Prolactin Responses to Serotonergic
Challenges in Depression 611
21.6.3 Prolactin Secretion Following
Treatment of Depression 612
21.7 Melatonin 612
21.7.1 Melatonin and Seasonal Affective
Disorder 612
21.7.2 Relationship to the HPA Axis 612
21.8 Other Neuroendocrine Peptides 612
21.8.1 Opioid Peptides 612
21.8.2 Substance P 613
21.8.3 Arginine Vasopressin 613
21.8.4 Neurotensin and NPY 613
21.8.5 Cholecystokinin and Endogenous
Opioids 613
21.8.6 Leptin 614
21.9 Summary 614
References 615
Further Reading 620
CHAPTER 22
Premenstrual Dysphoric Disorder 621
B L Parry, S Nowakowski, L F Martinez, and S L Berga
22.1 Introduction 622
22.2 Diagnostic Issues 622
22.2.1 Clinical Phenomenology 622
22.2.2 Relationship to Depression 624
22.2.3 Risk Factors, Inheritance and
Relationship to Other Mood Disorders 624
22.2.3.1 Mood disorders 624
22.2.3.2 Familial factors 624
22.2.3.3 Other reproductive-related
mood disorders 625
22.2.3.4 Age 625
22.2.4 Cultural Aspects 625
22.3 Etiology 625
22.3.1 Biomedical Model 625
22.3.2 Neuroendocrine Control of the
Menstrual Cycle 626
22.3.2.1 Gonadal steroids/
gonadotropins 626
22.3.2.2 Neurovegetative signs and
psychophysiological responses 628
22.3.2.3 Neuroendocrine 628
22.3.2.4 Neurotransmitters: Serotonin,
norepinephrine, and GABA 630
22.3.2.5 (3-Endorphin 633
22.3.2.6 Other (PGs, CCK, alpha
asymmetry, brain metabolic
changes, acupuncture,
vitamins, electrolytes, and CO2
inhalation) 634
22.3.3 Chronobiological Hypotheses 634
22.3.4 Summary 636
22.3.5 Emergence of a Biopsychosocial Model 636
22.4 Treatment 637
22.4.1 The Future 640
References 640
CHAPTER 23
Post-Traumatic Stress Disorder 649
R Yehuda and C Sarapas
23.1 Introduction 650
23.2 Cortisol Levels in PTSD 651
23.2.1 Twenty-Four-Hour Urinary Excretion
of Cortisol 651
23.2.2 Single-Time-Point Estimates of Basal
Cortisol 652
23.2.3 Circadian Rhythm of Cortisol 653
23.2.4 Cortisol Levels in Response to Stress 653
23.2.5 Cortisol as a Pretraumatic Risk Factor 654
23.3 CRF and ACTH Release in PTSD:
Baseline Studies 655
23.3.1 Corticotropin-Releasing Factor 655
23.3.2 Adrenocorticotropin Hormone 655
23.4 Endocrine Challenge Findings
Implicating CRF Hypersecretion in
PTSD 656
23.4.1 The Metyrapone Stimulation Test 656
23.4.2 CRF Challenge Findings 656
23.4.3 Cholecystokinin Tetrapeptide
Challenge Findings 657
23.5 The Dexamethasone Suppression Test
and Glucocorticoid Receptors in PTSD 657
23.5.1 The Dexamethasone Suppression Test 657
23.5.2 The Combined DEX/CRF Test 659
23.5.3 Glucocorticoid Receptors 659
23.5.4 Effects of Exogenous Cortisol
Administration 660
23.6 Putative Models of HPA-Axis
Alterations in PTSD 660
23.7 Conclusions 660
References 661
CHAPTER 24
Anorexia Nervosa and Bulimia Nervosa 665
G J Paz-Filbo and J Licitiio
24.1 Overview 665
24.2 Clinical Presentation 666
24.2.1 Anorexia Nervosa 666
24.2.2 Bulimia Nervosa 668
24.3 Hormonal Findings G68
24.3.1 Reproductive System 668
24.3.2 Thyroid Gland 669
Contents xvii
24.3.3 Adrenal Gland 670
24.3.4 Growth Hormone 670
24.3.5 Bone Metabolism 670
24.3.6 Leptin 670
24.3.7 Glucose Homeostasis 671
24.3.8 Other Endocrine Systems 672
24.4 Multifactorial Etiology 673
24.4.1 Functional Studies 673
24.4.2 Genetics 674
24.5 Endocrine Treatment 674
24.6 Conclusion 675
References 675
CHAPTER 25
Aging and Alzheimer s Disease 683
S J l.upitn, C Lord, S Sintli, ( . II II ilkinsim, imtl A J Viacca
25.1 Introduction 684
25.1.1 Diagnosis of AD 684
25.1.2 Pathophysiologyof AD 685
25.1.3 Clinical Features of AD 685
25.1.4 Stages of AD 685
25.1.5 Mild Cognitive Impairment: Between
Norn) and Pathology 686
25.2 Hormones, Aging, and AD 686
25.2.1 A Brief History on Hormones and AD 687
25.3 Gonadal Hormones 687
25.3.1 Gonadal Hormones and
Neuroprotection 687
25.3.1.1 Estrogen neuroprotection 687
25.3.1.2 Testosterone neuroprotection 688
25.3.2 Gonadal Hormones and Risk of AD 688
25.3.2.1 Estrogen and risk 688
25.3.2.2 Testosterone and risk 690
25.3.3 Gonadotropins 690
25.3.4 Gonadal Hormones: Prevention and
Treatment 690
25.3.4.1 Estrogen 690
25.3.4.2 Testosterone 691
25.4 Adrenal Hormones 691
254.1 Glucocorticoids 692
25.4.1.1 GCs and risk of AD 693
25.4.1.2 GCs: Prevention and treatment 693
25.4.2 Dihydroepiandrosterone 694
25.4.2.1 DHEA and risk of AD 694
25.4.2.2 Dihydroepiandrosterone:
Prevention and treatment 695
25.4.3 Catecholamines 695
25.4.3 1 Epinephrine 695
25.4.3.2 Norepinephrine 696
25.5 Insulin 698
25.5.1 Insulin and Cognition 698
25.5.2 Insulin and Diabetes: Risk for AD 698
xviii Contents
25.5.3 Insulin: Prevention and Treatment 699
25.5.3.1 Nonpharmacological
interventions 699
25.5.3.2 Pharmacological interventions 700
25.6 Melatonin 700
25.6.1 Melatonin and Aging 700
25.6.2 Melatonin Deficiency and Risk of AD 701
25.6.3 Melatonin: Prevention and Treatment 701
25.7 Genes, Hormones, and AD 702
25.7.1 Glucocorticoid Receptor
Polymorphism 702
25.7.2 Apolipoprotein E Gene and Hormone
Modulation 702
25.7.3 COMT Gene 702
25.7.4 Estrogen Receptor Genes 703
25.8 Conclusion 703
References 704
CHAPTER 26
Genetic Defects of Female Sexual
Differentiation 715
A B Desserts, M B C M Cools, A Richter-Vnruh, L H J
Looijenga, J A Grootegoed, and S L S Drop
26.1 Introduction 716
26.2 Ovarian and Female Development 717
26.2.1 Primary Sex Determination: Sex
Chromosomes Dictate Gonadal Sex 717
26.2.2 Ovarian Development: Orchestrated by
Ovary-Determining Genes? 718
26.2.3 Secondary Sex Determination:
Gonadal Hormones and the Sexual
Phenotype 720
26.2.4 Sex Differentiation of the Brain: Genes
versus Hormones 721
26.3 Sex Chromosomal Disorders of Sex
Development and Female Development 721
26.3.1 Incidence and Origin of 45,X/46,XY
Mosaicism 721
26.3.2 Phenotypic Spectrum of 45,X/46,XY
Mosaicism 722
26.3.3 Gonadal Histology, Tumor Risk, and
Fertility 722
26.3.4 Diagnosis and Treatment 724
26.4 Disorders of Androgen Excess 725
26.4.1 Fetal Origin 725
26.4.1.1 21-Hydroxylase deficiency 725
26.4.1.2 11-Beta hydroxylase deficiency 725
26.4.1.3 Steroidogenic acute regulatory
protein mutations 725
26.4.1.4 17-Alpha-hydroxylase and 21-
hydroxylase deficiency 727
26.4.1.5 CYP17Al/17,2O-lyase
deficiency 727
26.4.1.6 Glucocorticoid resistance 727
26.4.2 Fetoplacental Origin 729
26.4.2.1 Aromatase deficiency 729
26.4.3 Maternal Origin 729
26.4.3.1 Luteoma of pregnancy 729
26.5 Mullerian Agenesis/Hypoplasia
Syndromes 730
26.6 Effects of Gonadal Steroids on Brain
and Behavior 731
26.6.1 Role of Pre- and Postnatal Androgen
Exposure 731
26.6.2 Effects of Androgens on Sexuality 731
26.6.2.1 Gender role behavior 731
26.6.2.2 Sexual orientation and sexual
functioning 732
26.6.2.3 Gender identity 733
26.6.3 Roles of Androgens on Activity 734
26.6.4 Roles of Androgens on Aggression 734
26.6.5 Role of Androgens on Cognitive
Capacities 734
26.6.6 Role of Prenatally Elevated Amounts of
Estrogens on Behavior 735
26.6.7 Concluding Remarks 735
References 736
CHAPTER 27
Genetic Defects of Male Sexual
Differentiation 743
Y-S Zbu and J Imperato-McGinley
27.1 Introduction 744
27.2 Embryology of Male Sexual
Differentiation and Development 744
27.2.1 Formation of the Bipotential Gonad 744
27.2.2 Testicular Differentiation 745
27.2.3 Ovarian Differentiation 745
27.2.4 Ductal Differentiation 745
27.2.5 Differentiation of the External
Genitalia 745
2 7.3 The Genetic and Hormonal Control of
Male Sexual Differentiation 745
27.3.1 The Genetic Control of Testicular
Differentiation 746
27.3.2 Testicular Function 747
27.3.2.1 Testosterone production 747
27.3.2.2 Anti-Miillerian hormone 747
27.3.3 Enzymes and Genes Involved in
Testosterone Biosynthesis 747
27.3.3.1 StAR protein 748
27.3.3.2 Cholesterol 20,22-desmolase 748
27.3.3.3 3p -Hydroxysteroid
dehydrogenases 748
27.3.3.4 17a-Hydroxylase/17,20-
desmolase 749
27.3.3.5 17P-Hydroxysteroid
dehydrogenase 750
27.3.3.6 P450 oxidoreductase 750
27.3.4 Androgens and Target-Organ
Responsiveness 752
27.3.4.1 The enzyme 5 x-veductase-2 752
27.3.4.2 The androgen receptor 753
27.3.5 Summary 756
27.4 Disorders of Male Sexual
Differentiation Due to
Defects in Androgen Production
or Action 756
27.4.1 17PHSD3 Deficiency 756
27.4.1.1 The clinical syndrome of
17PHSD3 deficiency 756
27.4.1.2 Biochemical characterization
of 17PHSD3 deficiency 757
27.4.1.3 The molecular genetics of
17PHSD3 deficiency 758
27.4.2 5a-Reductase-2 Deficiency 758
27.4.2.1 The clinical syndrome of
5aRD2 deficiency 758
27.4.2.2 Biochemical characterization
of 5aRD2 deficiency 760
27.4.2.3 Molecular genetics of 5aRD2
deficiency 761
27.4.3 Androgen Insensitivity Syndrome 762
27.4.3.1 The androgen insensitivity
syndrome 762
27.4.3.2 The biochemical
characterization of androgen
insensitivity syndrome 762
27.4.3.3 Molecular genetics of androgen
insensitivity syndrome 762
27.5 Gender Identity Development 764
27.5.1 Social Theory in Gender Development 764
27.5.2 Hormone-Influence Theory in Gender
Development 764
27.5.3 Genetic Factors on Gender
Development 765
27.6 Gender Identity in Specific Inherited
Disorders Affecting Androgen
Biosynthesis and Androgen Actions 765
27.6.1 Gender Identity in Subjects with
5aRD2 Deficiency 765
27.6.2 Gender Identity in Subjects with
17PHSD3 Deficiency 768
27.7 Sex Differences in Cognitive Function
and Laterality 769
27.7.1 Cognitive Abilities in
Androgen-Insensitive Subjects 771
27.7.2 Other Studies of Cognitive Function in
Hypogonadal Males 772
Contents xix
27.8 Conclusion 773
References 773
CHAPTER 28
Assisted Reproduction in Infertile Women 781
/. Baor
28.1 Socio-Cultural Norms Regarding
Parenthood and Infertility 781
28.2 Assisted Reproductive Technologies 782
28.2.1 ART Medications 782
28.2.1.1 GnRH agonists 782
28.2.1.2 Mechanism of action 782
28.2.2 Gonadotropins 782
28.2.3 ART Procedure 783
28.2.3.1 Cycle preceding ART cycle 783
28.2.3.2 ART cycle 783
28.3 Psychological Reaction to Infertility 783
28.3.1 Loss of Relationship with Spouse 783
28.3.2 Loss of Sexual Satisfaction 783
28.3.3 Loss of Relationship within the Social
Network 784
2H..V4 Loss of Health 7H4
28.3.5 Loss of Status and/or Prestige 784
28.3.6 Lossof Self-Ksteem 784
28.3.7 Loss of Confidence and/or Control 784
28.3.8 Loss of Security 785
28.3.9 Loss of Hope 785
28.4 Multiple Pregnancy as a Side Effect
ofART 785
28.5 Psychological Reaction to Multiple
Parenthood 786
28.6 Parenting Preterm Multiples 787
28.7 Perinatal Death 787
28.8 Epilog 787
References 787
Further Reading 78V
CIIAPTKR . /
Transsexualism 791
R A Allison
29.1 Historical Perspective 791
29.2 Terminology 792
29.2 1 Transsexual versus Gender Identity
Disorder 792
29.2.2 Transsexualism versus Crossdressing 793
29.2.3 Transsexual versus Transgender 793
29.2.4 Primary versus Secondary 793
29.2.5 Sexual Orientation versus Gender
Identity 793
xx Contents
29.3 Hormone Treatment of Transsexual
Persons 793
29.4 Male-to-Female Hormone Treatment 794
29.4.1 Effects of Hormone Treatment in
Male-to-Female Transsexual Persons 794
29.4.2 Limitations of Estrogen Therapy 795
29.4.3 Side Effects of Estrogen Therapy 795
29.5 Female-to-Male Hormone Treatment 796
29.5.1 Effects of Testosterone Therapy 796
29.5.2 Limitations of Testosterone Therapy 796
29.6 The Social and Emotional Challenges
of Gender Transition 796
29.7 Conclusion 797
References 797
Further Reading 797
CHAPTER 30
Disorders of Salt and Fluid Balance 799
T Lenbard, M Bettendorf, and S Schwab
30.1 Physiology of Salt and Fluid Balance 800
30.1.1 Salt and Fluid Balance in the Kidney:
Normal Conditions 801
30.1.1.1 Structure of the nephron 801
30.1.1.2 Mechanisms of urine
concentration 801
30.1.2 Regulation of Fluid and Salt Balance 805
30.1.3 Symptoms of Disturbed Salt and Water
Balance 807
30.1.3.1 Hyponatremia 807
30.1.3.2 Excessive renal loss of water 808
30.2 Diabetes Insipidus 809
30.2.1 Nephrogenic Diabetes Insipidus 809
30.2.1.1 Aquaporin-associated
nephrogenic diabetes insipidus 809
30.2.1.2 AVP V2 receptor defects: X-
linked nephrogenic diabetes
insipidus 810
30.2.1.3 Other forms of hereditary
nephrogenic diabetes insipidus 811
30.2.1.4 Nongenetic causes of
nephrogenic diabetes insipidus 811
30.2.2 Central Diabetes Insipidus 811
30.2.2.1 Destruction of AVP-producing
neurons 811
30.2.2.2 Autoimmune pathology 812
30.2.2.3 Familial neurohypophyseal
diabetes insipidus 812
30.2.2.4 Primary polydipsia 812
30.2.3 Diagnostic Management of Polydipsia
and Polyuria 813
30.2.4 Treatment Options for Diabetes
Insipidus 814
30.3 Dysregulation of Salt and Fluid Balance
in Brain Disease 815
30.3.1 Cerebral Salt-Wasting Syndrome 815
30.3.1.1 Clinical presentation of CSWS 816
30.3.1.2 Etiology of CSWS 817
30.3.1.3 Pathophysiological concepts of
CSWS 819
30.3.2 Syndrome of Inappropriate
Antidiuresis 821
30.3.2.1 PathophysiologyofSIAD 821
30.3.2.2 Conditions favoring SIAD 822
30.3.3 Clinical Differentiation and Treatment
of Hyponatremia 823
30.3.3.1 Diagnosis of CSWS and SIAD 823
30.3.3.2 Therapy of hyponatremia in
CSWS and SIAD 824
References 827
Further Reading 829
CHAPTER 31
Diabetes Mellitus and Neurocognitive
Dysfunction 831
C M Ryan
31.1 Introduction 832
31.2 Clinical Syndromes of Diabetes
Mellitus 832
31.2.1 Type 1 Diabetes 832
31.2.2 Type 2 Diabetes 833
31.3 Neurocognitive Phenotypes 833
31.3.1 Adults with Type 1 Diabetes 834
31.3.1.1 Cognitive manifestations 834
31.3.1.2 Electrophysiological changes 835
31.3.1.3 Cerebrovascular outcomes 836
31.3.1.4 Brain structure anomalies 837
31.3.1.5 Alterations in brain metabolites 838
31.3.2 Children and Adolescents with Type 1
Diabetes 838
31.3.2.1 Cognitive manifestations 838
31.3.2.2 Electrophysiological changes 840
31.3.2.3 Cerebrovascular outcomes 840
31.3.2.4 Brain structure anomalies 841
31.3.2.5 Alterations in brain metabolites 842
31.3.3 Adults with Type 2 Diabetes 842
31.3.3.1 Cognitive manifestations 842
31.3.3.2 Electrophysiological changes 843
31.3.3.3 Cerebrovascular outcomes 844
31.3.3.4 Brain structure anomalies 845
31.3.3.5 Alterations in brain metabolites 846
31.3.4 Diabetes-Associated Neurocognitive
Phenotypes: One or Many? 847
31.4 Biomedical Risk Factors 847
31.4.1 Hypoglycemia 848
31.4.1.1 CNS effects of extended
episodes of profound
hypoglycemia 848
31.4.1.2 Do single or recurrent episodes
of less severe hypoglycemia
have neurocognitive sequelae? 848
31.4.2 Chronic Hyperglycemia 849
31.4.2.1 Clinically significant
microvascular complications
predict cognitive impairment 849
31.4.2.2 Retinopathy as a surrogate
marker of cerebral
microangiopathy 850
31.4.2.3 Chronic hyperglycemia may
interfere with normal brain
development 850
31.5 Pathophysiological Mechanisms 851
31.5.1 Glucose Toxicity 851
31.5.2 Hyperglycemia, Insulin Dysregulation,
and Brain Dysfunction 851
31.6 Diabetes and Brain Dysfunction: Some
Final Thoughts 852
References 853
CHAPTER 32
Alcohol Abuse: Endocrine Concomitants 863
E S Ginsburg, N K Mello, and J H Mendelson
32.1 Introduction 864
32.2 Alcohol and Reproductive System
Dysfunction in Women 865
32.2.1 Overview of Effects of Alcohol on
Reproductive Function 865
32.2.1.1 Anovulation and luteal-phase
dysfunction in alcoholic
women 865
32.2.1.2 Anovulation and luteal-phase
defects in social drinkers 865
32.2.1.3 Amenorrhea 866
32.2.2 Effects of Alcohol on Hypothalamic,
Pituitary, Gonadal, and Adrenal
Hormones 867
32.2.2.1 Provocative tests of hormonal
function 867
32.2.2.2 Follicular phase 868
32.2.2.3 Amenorrhea and gonadotropin
secretory activity 869
32.2.2.4 Effects of alcohol on ovarian
hormones during the follicular
phase 870
32.2.2.5 Luteal phase 871
32.2.3 Corticotropin-Releasing Factor 873
32.2.3.1 Mechanisms of alcohol effects
on the pituitary-adrenal axis 874
32.2.4 Prolactin 874
32.2.4.1 Hyperprolactinemia and
alcohol-related amenorrhea 875
32.2.4.2 Acute effects of alcohol on
prolactin 875
Contents xxi
32.2.4.3 Luteal-phase dysfunction and
prolactin abnormalities:
Possible mechanisms 876
32.3 Alcohol Effects in Postmenopausal
Women 876
32.3.1 Alcohol Effects in Postmenopausal
Women Not on HRT 876
32.3.1.1 Acute alcohol effects on the
hypothalamic-pifuitary-
gonadal or adrenal axis 876
32.3.1.2 Chronic alcohol effects on the
hypothalamic-pituitary-
gonadal or adrenal axis 877
32.3.2 Alcohol Effects in Postmenopausal
Women on Estrogen Replacement
Therapy 878
32.3.2.1 Acute alcohol effects:
Gonadotropin and ovarian
steroid hormones 878
32.3.2.2 Chronic alcohol effects:
Estrogen and breast cancer 878
32.4 Implications of Stimulatory Effects of
Alcohol on Pituitary and Gonadal
Hormones K7(
32.5 Implications of Alcohol-Induced
Changes in Maternal Reproductive
Hormones for Pregnancy and Fetal
Growth and Development 87°
32.5.1 Ovarian Steroid Hormones and
Teratogenesis 880
32.5.2 Hypothalamic-Pituitary-Adrenal
Factors in Teratogenesis 881
32.5.3 Alcohol Use and Spontaneous Abortion 882
32.5.4 Alcohol and Reproductive System
Development 883
32.5.5 Alcohol Abuse and Teratogenesis:
The FAS 883
32.5.5.1 Animal models of FAS 883
32.5.5.2 Possible mechanisms of FAS 884
32.5.6 Polydrug Abuse 885
32.6 Effects of Alcohol on Hormone
Function in Men 885
32.6.1 Testosterone 885
32.6.2 Gonadal Steroids and Provocative
Testing 886
32.6.2.1 Luteinizing hormone-releasing
hormone/follicle-stimulating
hormone/luteinizing hormone 886
32.6.2.2 CRH/adrenocorticotropic
hormone/cortisol 887
32.6.2.3 Adrenocorticotropic hormone 887
32.6.2.4 Prolactin 888
32.6.3 Thyroid Hormones 888
32.6.4 Mechanisms of Alcohol-Related
Hormonal Changes in Men 888
xxii Contents
32.7 Conclusions 888
References 888
Further Reading 897
CHAPTER 33
Effects of Smoking on Hormones, Brain, and
Behavior 899
T Sidhartha, R E Poland, and U Rao
33.1 Introduction 899
33.2 Hypothalamic-Pituitary-Adrenal Axis 900
33.2.1 Acute Response of the HPA Axis to
Smoking 900
33.2.2 HPA Axis in Chronic Smokers 901
33.2.3 Mechanism of HPA Activation by
Nicotine 901
33.2.4 Smoking, Mental Illness, and the
HPA Axis 902
33.2.4.1 Smoking, depression, and the
HPA axis 902
33.2.4.2 Schizophrenia, smoking, and
the HPA axis 903
33.2.4.3 Anxiety disorders, smoking and
the HPA axis 904
33.2.5 HPA Response to Stress in Smokers 904
3 3.2.6 HPA Changes Associated with Nicotine
Addiction 906
33.2.6.1 Brain regions involved in
nicotine addiction and
regulation of HPA axis 907
33.2.7 Nicotinic Acetylcholinergic Receptors 908
33.2.7.1 Smoking, anxiety, and nicotinic
acetylcholinergic receptors 908
33.2.7.2 Nicotinic acetylcholinergic
receptors and schizophrenia 909
33.2.7.3 Nicotinic acetylcholinergic
receptors and depression 910
33.2.8 Smoking and Other Pituitary
Hormones 911
33.3 Thyroid Hormone 911
33.4 Sex Hormones 912
33.5 Smoking and Insulin Resistance 914
33.6 Smoking and Osteoporosis 914
33.7 Summary 915
References 916
CHAPTER 34
Cocaine, Hormones and Behavior 925
N K Melto and J H Mendelson
34.1 Introduction 925
34.2 Cocaine s Effects on ACTH and
Cortisol/Corticosterone 926
34.2.1 Background 926
34.2.2 Clinical Studies of the Acute Effects of
Cocaine on ACTH and Cortisol 927
34.2.2.1 Acute effects of cocaine on
basal levels of ACTH and
cortisol 927
34.2.2.2 Acute effects of cocaine on
pulsatile release of ACTH 928
34.2.3 Clinical Studies of Chronic Cocaine
Effects on ACTH and Cortisol 929
34.2.4 Clinical Studies of the HPA Axis and
Cocaine s Behavioral Effects 930
34.2.4.1 CRH antagonists:
Development and behavioral
implications 932
34.3 Cocaine s Effects on Gonadotropins
and Gonadal Steroid Hormones 934
34.3.1 Background 934
34.3.1.1 Changes in gonadotropin and
gonadal steroid hormone levels
across the menstrual cycle 934
34.3.1.2 Interactions between
gonadotropins and gonadal
steroid hormones 935
34.3.1.3 Regulation of pulsatile
gonadotropin release patterns 935
34.3.2 Clinical Studies of Cocaine Effects on
Gonadotropin Hormones 936
34.3.2.1 Acute effects of cocaine on LH
in men and women 936
34.3.3 Clinical Studies of Chronic Cocaine
Effects on LH 937
34.3.3.1 Implications of cocaine s
stimulation of LH 937
34.4 Interactions between Cocaine, Sex, and
Gonadal Steroid Hormones 939
34.4.1 Background 939
34.4.2 Interactions between Cocaine, Sex, and
Menstrual-Cycle Phase 941
34.4.2.1 Sex, menstrual-cycle phase,
and cocaine pharmacokinetics 941
34.4.2.2 Sex, menstrual-cycle phase,
and neuroimaging studies 942
34.4.2.3 Sex, menstrual-cycle phase,
and cocaine s subjective effects 942
34.5 Effects of Cocaine on Reproductive
Function 945
34.5.1 Background 945
34.5.2 Studies of the Effects of Chronic
Cocaine Administration on
Reproductive Function 947
34.6 Conclusions 950
References 951
Further Reading 959
CHAPTER 35
Short-Acting Opiates vs. Long-Acting
Opioids 961
M J Kreek, L Borg, Y Zhou, and I Kravets
35.1 Laboratory Research Update and
Overview 961
35.1.1 Hypothalamic-Pituitary-Adrenal Axis 961
35.1.2 Steady-State Methadone by
Osmotic Pumps Decreases
Cocaine-Seeking Behavior in Animal
Models 962
35.1.3 Involvement of n-Opioid Receptor,
Orexin, and Preprodynorphin Gene
Expression in the Lateral
Hypothalamus in Animal Models of
Opioid Dependence 963
35.1.4 Involvement of Arginine Vasopressin
and Vlb Receptor in Drug Withdrawal
and Heroin Seeking Precipitated by
Stress and by Heroin 963
35.2 Clinical Research Update and
Overview 964
35.2.1 Clinical Studies of Pharmacokinetics of
Heroin and Morphine as Contrasted
with Methadone 968
35.2.2 Clinical Studies of HPA Axis 969
35.2.3 Tuberoinfundibular Dopaminergic/
Prolactin System Interactions 978
35.2.4 Hypothalamic-Pituitary-Gonadal Axis 980
35.2.5 Growth Hormone and Opioid
Addiction 980
35.2.6 Thyroid Function and Opioid
Addiction 980
35.2.7 |i-Opioid Receptor Binding in Healthy
Normal and Methadone-Maintained
Volunteers 980
35.2.8 Human Molecular Genetics of Heroin
Addiction of the Endogenous Opioid
Systems and Polymorphisms of Genes 982
References 984
CHAPTER 36
Pain: Sex/Gender Differences 991
A Z Murphy, KJ Berkley, and A Holdcrofi
36.1 Overview 2
36.2 Pain: A Summary 992
36.2.1 What Is Pain? 992
36.2.2 How Is Pain Classified? 992
36.2.3 How Is Pain Measured? 993
36.2.4 What Are the Mechanisms of Pain? 994
36.2.5 How Is Pain Managed? 994
36.3 Sex Differences in Pain 994
36.3.1 Pain, Epidemiology, and Sex/Gender
Differences 4
Contents xxiii
36.3.2 Pain, Nociception, and Sex/Gender
Differences 995
36.3.3 Pain Therapies and Sex/Gender
Differences 996
36.4 Pain Mechanisms and Sex/Gender
Differences 996
36.4.1 Genetics 997
36.4.2 Body Physiology and Structure 997
36.4.2.1 Physiology: General 997
36.4.2.2 Physiology: Cardiovascular
system as an example 997
36.4.3 Pelvic Organs 998
36.4.4 Brain Function 999
36.5 The Influence of Sex Steroid Hormones
on Pain and Nociception 999
36.5.1 Potential Mechanisms: The
Descending Pain Modulatory Circuit 1000
36.6 Stress and Pain 1001
36.7 Life Span Events, Lifestyle, and
Sociocultural Roles 1001
36.7.1 Fetus, Childhood, and Puberty 1001
36.7.2 Fertile Adulthood 1002
36.7.3 (jonadal Aging and Senescence 1002
36.8 Clinical Implications 1003
36.8.1 The Diagnostic Process 1003
36.8.2 PharmaceuticalTherapies 1003
36.8.2.1 Adverse drug events 1004
36.8.2.2 Drug development 1004
36.8.2.3 Drug selection 1004
36.8.2.4 Sex differences in short- and
longer-term effects of opioids 1004
36.8.2.5 Physical interventions 1005
36.8.2.5 Situational manipulations 1005
36.8.2.6 Advantages of varying and
combining therapies 1005
36.8.3 Hormones, Pain and the Clinic: Two
Examples 1006
36.8.3.1 Diabetes 1006
36.8.3.2 Coronary artery disease 1006
36.9 Conclusion 1007
References 1007
Further Reading 1012
CHAFTKR
Traumatic Brain Injury 1013
B E Masel and R Temple
37.1 Incidence 1013
37.2 Anatomy and Physiology of the
Pituitary and Hypothalmus 1014
37.3 Prevalence Studies 1016
37.3.1 Acute TBI 1016
37.3.2 Chronic TBI 1016
xxiv Contents
37.4 PediatricTBI 1017
37.5 Imaging Following TBI 1017
37.6 Pituitary Hormones 1017
37.6.1 Prolactin 1017
37.6.2 Thyroid Hormone 1019
37.6.3 Thyroid Hormone and Cognition 1019
37.6.4 Steroids 1019
37.6.5 Gonadotropins 1020
37.6.6 Growth Hormone 1021
37.6.7 Diagnosis and Treatment 1021
37.6.8 Treatment of GHD 1021
37.6.9 Metabolic Effects of GHD 1021
37.6.10 Metabolic Effects of GH
Replacement 1022
37.6.11 Cognitive Impact of Post-Traumatic
GHD 1022
37.6.12 Cognitive Impact of GH Replacement 1023
37.7 Posterior Pituitary Dysfunction
Following TBI 1023
37.7.1 Arginine Vasopressin 1024
37.7.2 Diabetes Insipidus 1024
37.7.3 Syndrome of Inappropriate
Antidiuretic Syndrome 1024
37.7.4 Incidence of Posterior Pituitary
Dysfunction 1024
37.8 Treatment 1024
37.8.1 When to Screen 1024
37.8.2 How to Screen 1024
37.8.3 When to Treat 1025
37.9 Symptoms of a TBI and PTH 1025
References 1026
CHAPTER 38
Human Immunodeficiency Virus and AIDS 1029
Y Miyasaki, M B Goetz, and T F Newton
38.1 Human Immunodeficiency Virus
Natural History 1030
38.1.1 Clinically Latent Period 1030
38.1.2 CD4+ Cell Count versus Clinical
Complications of HIV Infection 1030
38.2 Primary Neuropsychiatric Disorders
Related to HIV Infection per se 1031
38.2.1 Neuropsychiatric Syndromes during
Acute HIV Seroconversion Reactions 1031
38.2.2 Neurocognitive Impairment Associated
with HIV Infection 1031
38.2.2.1 Clinical manifestations of HAD 1032
38.2.2.2 Diagnostic strategies and
therapeutic considerations 1032
38.3 Secondary Neuropsychiatric Processes
Related to HIV Infection 1032
38.3.1 Adverse Neuropsychiatric Side Effects
of Medications Used in the Treatment
of HIV-Infected Individuals 1033
38.4 Specific Endocrinological
Complications 1033
38.4.1 Adrenocortical Dysfunction 1033
38.4.1.1 Adrenal insufficiency
(Addison s disease) 1033
38.4.1.2 Adrenal excess and Cushing s
syndrome 1034
38.4.1.3 Common iatrogenic causes of
adrenal disease in HIV-infected
patients 1035
38.4.1.4 Clinical manifestations of
adrenal insufficiency and
excess in HIV-infected patients 1035
38.4.1.5 Diagnostic strategies and
therapeutic considerations 1035
38.4.2 Gonadal Dysfunction 1036
38.4.2.1 Hypogonadism 1036
38.4.2.2 Common iatrogenic causes of
hypogonadism in HIV-infected
patients 1036
38.4.2.3 Clinical manifestations of
hypogonadism in HIV-infected
patients 1037
38.4.2.4 Diagnostic strategies and
therapeutic considerations 1037
38.4.3 Thyroid Hormone Abnormalities 1038
38.4.3.1 HIV-related hypothyroidism 1038
38.4.3.2 HIV-related hyperthyroidism 1039
38.4.3.3 Common iatrogenic causes of
thyroid disease in HIV-infected
patients 1039
38.4.3.4 Clinical manifestations of
hypothyroidism in HIV-
infected patients 1039
38.4.3.5 Diagnostic strategies and
therapeutic considerations 1039
38.4.4 Morphologic and Metabolic
Abnormalities in HIV-Infected Patients 1039
38.4.4.1 Neuropsychiatric impact of LD
in HIV-infected patients 1040
38.4.4.2 Diagnostic strategies and
therapeutic considerations 1041
References 1041
Further Reading 1047
Index 1049
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| format | Book |
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| id | DE-604.BV036092988 |
| illustrated | Illustrated |
| indexdate | 2024-07-09T22:11:24Z |
| institution | BVB |
| isbn | 9780123749260 |
| language | English |
| oai_aleph_id | oai:aleph.bib-bvb.de:BVB01-018983557 |
| oclc_num | 317674309 |
| open_access_boolean | |
| owner | DE-91 DE-BY-TUM DE-355 DE-BY-UBR DE-11 |
| owner_facet | DE-91 DE-BY-TUM DE-355 DE-BY-UBR DE-11 |
| physical | XXIX, 1152 S. Ill., graph. Darst. |
| publishDate | 2009 |
| publishDateSearch | 2009 |
| publishDateSort | 2009 |
| publisher | Elsevier [u.a.] |
| record_format | marc |
| spelling | Hormone - behavior relations of clinical importance endocrine systems interacting with brain and behavior ed. by Robert T. Rubin ... Amsterdam [u.a.] Elsevier [u.a.] 2009 XXIX, 1152 S. Ill., graph. Darst. txt rdacontent n rdamedia nc rdacarrier Includes bibliographical references and index Human behavior Endocrine aspects Psychoneuroendocrinology Psychoendokrinologie (DE-588)4122321-4 gnd rswk-swf Psychopathologie (DE-588)4047724-1 gnd rswk-swf Psychology, Pathological Endocrine glands / Diseases Molecular endocrinology Human behavior / Endocrine aspects Psychoendokrinologie (DE-588)4122321-4 s Psychopathologie (DE-588)4047724-1 s DE-604 Rubin, Robert T. Sonstige oth HBZ Datenaustausch application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=018983557&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis |
| spellingShingle | Hormone - behavior relations of clinical importance endocrine systems interacting with brain and behavior Human behavior Endocrine aspects Psychoneuroendocrinology Psychoendokrinologie (DE-588)4122321-4 gnd Psychopathologie (DE-588)4047724-1 gnd |
| subject_GND | (DE-588)4122321-4 (DE-588)4047724-1 |
| title | Hormone - behavior relations of clinical importance endocrine systems interacting with brain and behavior |
| title_auth | Hormone - behavior relations of clinical importance endocrine systems interacting with brain and behavior |
| title_exact_search | Hormone - behavior relations of clinical importance endocrine systems interacting with brain and behavior |
| title_full | Hormone - behavior relations of clinical importance endocrine systems interacting with brain and behavior ed. by Robert T. Rubin ... |
| title_fullStr | Hormone - behavior relations of clinical importance endocrine systems interacting with brain and behavior ed. by Robert T. Rubin ... |
| title_full_unstemmed | Hormone - behavior relations of clinical importance endocrine systems interacting with brain and behavior ed. by Robert T. Rubin ... |
| title_short | Hormone - behavior relations of clinical importance |
| title_sort | hormone behavior relations of clinical importance endocrine systems interacting with brain and behavior |
| title_sub | endocrine systems interacting with brain and behavior |
| topic | Human behavior Endocrine aspects Psychoneuroendocrinology Psychoendokrinologie (DE-588)4122321-4 gnd Psychopathologie (DE-588)4047724-1 gnd |
| topic_facet | Human behavior Endocrine aspects Psychoneuroendocrinology Psychoendokrinologie Psychopathologie |
| url | http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=018983557&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA |
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