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  • 1
    Online Resource
    Online Resource
    San Diego :Elsevier Science & Technology,
    Keywords: Brain-Effect of stress on. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (272 pages)
    Edition: 1st ed.
    ISBN: 9780128211175
    Series Statement: Issn Series
    DDC: 616.8
    Language: English
    Note: Intro -- Stress and Brain Health: In Clinical Conditions -- Copyright -- Contents -- Contributors -- Chapter One: Stress, the brain, and trauma spectrum disorders -- 1. Lasting effects of traumatic stress -- 2. Trauma spectrum disorders -- 3. Psychologic trauma at various levels of development -- 4. A psycho-evolutionary view of stress, the brain, and neuropsychiatric disorders -- 5. Neurohormonal responses to trauma -- 6. The neural circuitry of PTSD -- 7. Conclusions -- Acknowledgment -- References -- Chapter Two: Is there neuroinflammation in depression? Understanding the link between the brain and the peripheral immune ... -- 1. The immune pathway to the brain -- 2. Markers of neuroinflammation in depression -- 3. Is there microglia activation in depression? -- 3.1. Preclinical evidence -- 3.2. Post-mortem studies -- 4. Clinical studies -- 5. The importance of human models of the link between peripheral and brain inflammation -- 5.1. New potential measures of neuroinflammation -- 5.1.1. MRI techniques potential -- 6. Clinical implications -- 7. Conclusions -- Acknowledgment -- Conflicts of interest -- References -- Chapter Three: Chronic stress, structural exposures and neurobiological mechanisms: A stimulation, discrepancy and depriv ... -- 1. Introduction -- 1.1. Co-occurrence and convergence of structural exposures -- 1.2. Social drift -- 2. Converging mechanisms impacted by the three structural exposures -- 2.1. HPA dysregulation -- 2.2. Dopamine dysregulation -- 2.3. Glutamate dysregulation -- 2.4. Inflammation -- 2.5. Stimulation discrepancy deprivation model of psychosis -- 3. Stimulation structural exposure -- 3.1. Stimulation definition and relations to psychotic disorder risk -- 3.2. Stimulation intermediary mechanisms -- 3.3. Stimulation exposure neural mechanisms -- 4. Discrepancy structural exposure. , 4.1. Discrepancy definition and relations to psychotic disorder risk -- 4.2. Discrepancy intermediary mechanisms -- 4.3. Discrepancy neural mechanisms -- 5. Deprivation structural exposure -- 5.1. Deprivation definition and relations to psychotic disorder risk -- 5.2. Deprivation intermediary mechanisms -- 5.3. Deprivation neural mechanisms -- 6. Stimulation discrepancy deprivation model of psychosis summary -- 7. Future directions -- References -- Chapter Four: The influence of stress and early life adversity on addiction: Psychobiological mechanisms of risk and resi ... -- 1. Introduction and definitions -- 2. Stress response neurobiological pathways -- 3. Addiction and brain reward pathways -- 4. Stress and ELA as a risk factor for addiction -- 5. Mechanisms mediating effects of stress on addiction -- 5.1. Preclinical evidence on mechanisms mediating ELA and addiction -- 5.2. ELA and HPA blunted response in humans -- 5.3. Stress and mesolimbic DA functions -- 6. Moderators of the effects of stress and ELA on addiction -- 6.1. Genetic and epigenetic factors -- 6.2. Sex differences -- 6.3. Resilience and factors that may buffer effects of stress on addiction -- 7. Discussion and heuristic model -- 8. Future directions -- 9. Conclusion -- Acknowledgment -- Declarations of interest -- References -- Chapter Five: Stress, cortisol and suicide risk -- 1. Introduction -- 1.1. Stress-diathesis models of suicidal behavior -- 1.2. The integrated motivational-volitional model of suicidal behavior -- 2. Cortisol and suicide risk -- 2.1. The dexamethasone suppression test (DST) and suicide risk -- 2.2. Naturally fluctuating cortisol and suicidal behavior -- 2.3. Cortisol reactivity to laboratory stress and suicide behavior -- 3. Childhood trauma-Cortisol-Suicide risk -- 3.1. Childhood trauma and the hypothalamic-pituitary-adrenal axis. , 4. Possible mechanisms linking stress and suicide risk -- 4.1. Executive function and impulsivity -- 4.2. Family history -- 4.3. Perinatal influences and epigenetics -- 4.4. Sleep -- 5. General conclusion -- References -- Chapter Six: Stress and cortisol in Parkinson´s disease -- 1. Introduction -- 2. Stress as a risk factor for PD -- 3. Neurobiochemical and cortisol changes in relation to stress in PD -- 4. Psychological stress -- 4.1. The phenomenon of paradoxical kinesia in PD -- 5. HPA-axis abnormalities in PD and biological stress -- 5.1. Studies in animal models -- 5.2. The effect of HPA-axis abnormalities in PD -- 5.3. Pathophysiology of HPA-axis abnormalities and links with depression -- 5.4. Genetics and epigenetics -- 6. Cortisol as a target for treatment -- 7. Conclusions -- References -- Chapter Seven: The effects of stress on cardiovascular disease and Alzheimer´s disease: Physical exercise as a counteract ... -- 1. Introduction -- 2. Stress, cardiovascular disease and Alzheimer´s disease -- 2.1. Adrenal pituitary hypothalamic axis -- 2.2. Autonomic nervous system -- 3. Hypertension -- 4. Diabetes type 2 -- 5. Obesity -- 6. Exercise for stress, cardiovascular health, cognition and AD -- 6.1. Exercise and hypertension -- 6.2. Exercise and diabetes -- 6.3. Exercise and obesity -- 7. Conclusions -- References -- Further reading -- Chapter Eight: The intersections of stress, anxiety and epilepsy -- 1. Introduction -- 2. Classification of anxiety -- 3. Overlap of depression and anxiety -- 4. Anxiety as a peri-ictal phenomenon -- 5. Psychogenic nonepileptic events -- 6. Stress and epilepsy -- 6.1. Stress exacerbating epilepsy -- 6.2. New onset epilepsy resulting from stress -- 7. Anxiety and depression comorbidity in epilepsy -- 7.1. Anxiety in epilepsy -- 7.2. Depression in epilepsy -- 8. How the HPA axis contributes to comorbidity. , 9. Treatment strategies -- 9.1. Antidepressants -- 9.2. Benzodiazepines -- 10. Conclusion -- References -- Chapter Nine: Stress and the vestibular system -- 1. Basic introduction to the anatomy and physiology of the vestibular system -- 2. The physiology of vestibular compensation -- 3. Stress and the vestibular system -- 4. Vestibular deafferentation activates the stress axis -- 5. Stress axis activation can facilitate or impair vestibular compensation -- 6. Stress and vestibular function in man -- 7. Stress and vestibular compensation in man -- 8. Chronic stress and the poorly compensated patient -- 9. Balance, stress, anxiety and depression -- 10. Individuals factors, stress and balance -- 11. Future directions for research -- 12. Concluding remarks -- References -- Chapter Ten: Social prescribing for stress related disorders and brain health -- 1. Introduction -- 2. Stress and society -- 3. Social prescribing -- 3.1. Social prescribing and mental wellbeing -- 3.2. ``Green medicine´´ -- 4. Social prescribing: Service users´ perspectives -- 5. Social prescribing: Service providers´ experiences -- 5.1. Link workers -- 6. Conclusions -- References -- Further reading.
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  • 2
    Online Resource
    Online Resource
    San Diego :Elsevier Science & Technology,
    Keywords: Brain-Effect of stress on. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (258 pages)
    Edition: 1st ed.
    ISBN: 9780128167533
    Series Statement: Issn Series
    DDC: 616.8
    Language: English
    Note: Intro -- Stress and Brain Health: Across the Life Course -- Copyright -- Contents -- Contributors -- Chapter One: Salivary cortisol as a non-invasive window on the brain -- 1. Why is cortisol interesting? -- 2. What is cortisol? -- 3. Stress and its measurement -- 4. Salivary cortisol measurement in human studies -- 5. Stress reactivity studies -- 6. Basal pattern of salivary cortisol secretion -- 7. The ultradian pattern of cortisol secretion and the cortisol awakening response -- 8. Alternative strategies to probe brain function using salivary cortisol -- 9. Methodological issues when measuring basal salivary cortisol secretion -- 10. Conclusions -- References -- Chapter Two: Prenatal stress: Effects on fetal and child brain development -- 1. Introduction -- 1.1. Fetal programming -- 1.2. The fetal brain -- 2. Effects of prenatal stress on fetal brain development -- 2.1. Animal studies -- 2.2. Human studies -- 2.2.1. Structural MRI studies -- 2.2.2. Diffusion MRI studies -- 2.2.3. Functional MRI studies -- 2.3. Different types of stress -- 3. Underlying mechanisms -- 4. Conclusions -- References -- Chapter Three: The development of stress reactivity and regulation during human development -- 1. Anatomy and physiology of the HPA axis and its development -- 1.1. Developmental changes in the HPA axis and its regulation -- 1.1.1. Prenatal -- 1.1.2. Infancy and early childhood -- 1.1.3. Childhood and adolescence -- 1.2. Brain systems regulating stress and their development -- 1.2.1. Amygdala -- 1.2.2. Hippocampus -- 1.2.3. Medial prefrontal cortex (mPFC) -- 1.2.4. Chronic stress -- 2. Theoretical perspectives on stress and development -- 3. Sensitive periods -- 3.1. The prenatal period -- 3.2. The early postnatal period/infancy -- 3.3. Pubertal recalibration/adolescence -- 4. Social regulation of stress during development -- 4.1. Infancy. , 4.2. Childhood -- 4.3. Adolescence -- 5. Conclusions and future directions -- Acknowledgments -- References -- Further reading -- Chapter Four: The impact of childhood poverty on brain health: Emerging evidence from neuroimaging across the lifespan -- 1. Introduction -- 2. Lifespan perspective -- 3. Prenatal period and infancy -- 4. Childhood -- 5. Adolescence -- 6. Adulthood and late adulthood -- 7. Links to physical health, behavioral outcomes, and mental health -- 8. Risks and protective factors -- 8.1. Cumulative risk -- 8.2. Parenting interventions -- 9. Future directions -- 9.1. Network neuroscience -- 9.2. Population neuroscience -- 9.3. Utilizing multiple neuroimaging modalities -- 9.4. Longitudinal studies and mediation analysis -- 10. Conclusions -- References -- Further reading -- Chapter Five: Psychosocial stress and epigenetic aging -- 1. Chronological versus biological age -- 2. Epigenetic embedding of psychosocial stress -- 3. Exposure to life adversity accelerates epigenetic aging -- 4. Socioeconomic status and epigenetic aging -- 5. Developmental programming of epigenetic age at birth -- 6. Mechanistic insights of stress-mediated accelerated aging -- References -- Chapter Six: Effects of stress on the structure and function of the medial prefrontal cortex: Insights from animal models -- 1. Introduction -- 2. Effects of chronic stress on prefrontally-mediated behaviors -- 3. Effects of chronic stress on structure and function of the prefrontal cortex -- 3.1. Effects of chronic stress on the medial prefrontal cortex: Morphology -- 3.2. Effects of chronic stress on the medial prefrontal cortex: Physiology -- 3.3. Effects of chronic stress on medial prefrontal cortex: Neurochemistry -- 4. Long-term sequelae of chronic stress -- 5. Mechanisms of chronic stress-induced alterations in the medial prefrontal cortex. , 6. Sex differences in the effect of stress on the medial prefrontal cortex -- 7. Conclusions -- Conflict of interest statement -- References -- Chapter Seven: Environment and early life: Decisive factors for stress-resilience and vulnerability -- 1. The influence of early life stress in behavioral plasticity -- 2. A critical role of mother-infant interactions in mental health -- 3. Mechanisms of homeostasis, allostatic load, stress vulnerability, and resilience -- 4. Neuroendocrine systems regulating the stress response -- 5. Influences of differential early-life environment on brain function? -- 6. Environmental control of stress resilience -- 6.1. Maternal separation (MS) -- 6.2. Effects of MS on neuronal plasticity and molecules in the brain -- 6.3. Enriched environment (EE) -- 6.4. Effects of EE on neuronal plasticity and molecules in the brain -- 7. Conclusion -- Acknowledgment -- References -- Chapter Eight: Stress, the cortisol awakening response and cognitive function -- 1. Stress, cortisol and cognition -- 2. The cortisol awakening response -- 3. The suprachiasmatic nucleus -- 4. The circadian system and psychopathology -- 5. The CAR and cognition -- 6. The CAR and memory functions -- 7. The CAR and executive function -- 8. Recommendations for future research -- 9. Conclusion -- References -- Chapter Nine: Effectiveness of stress-relieving strategies in regulating patterns of cortisol secretion and promoting bra ... -- 1. Stress-disease and well-being-health links -- 2. Cortisol: Its role in health -- 3. Cortisol ``a window on the brain´´: A marker of brain health -- 3.1. Cortisol circadian rhythms: Chronic stress exposure -- 3.1.1. The cortisol awakening response (CAR) -- 3.2. The cortisol diurnal profile -- 3.3. Stress/cortisol responding -- 4. Stress-relieving strategies -- 4.1. Positive psychological interventions. , 5. Arts and music therapies -- 5.1. Mindfulness-based interventions -- 5.2. Yoga practice -- 5.3. Physical exercise -- 5.4. Nature and physical activity -- 5.5. The importance of enjoyment and engagement in stress-relieving activities -- 6. Conclusions -- References.
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  • 3
    Online Resource
    Online Resource
    San Diego :Elsevier Science & Technology,
    Keywords: Dreams. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (373 pages)
    Edition: 1st ed.
    ISBN: 9780123813237
    Series Statement: Issn Series
    Language: English
    Note: Cover -- International Review of Neurobiology -- Copyright -- Contents -- Contributors -- Preface -- The Development of the Science of Dreaming -- I. Results -- II. Conclusion -- Acknowledgments -- References -- Dreaming as Inspiration: Evidence from Religion, Philosophy,Literature, and Film -- I. Introduction -- II. Quality of Evidence -- III. Religion -- IV. Philosophy -- V. Literature -- VI. Film -- VII. Conclusion -- References -- Developmental Perspective: Dreaming Across the Lifespanand What This Tells Us -- I. Introduction -- II. Background and Clinical Perspective -- III. Sleep and Speculations about Dreaming in Infancy -- IV. Sleep and Dreaming in Childhoo -- V. Sleep and Dreaming in Adolescence -- VI. Sleep and Dreaming in Adulthood -- VII. Sleep and Dreaming in Older Adulthood -- VIII. Conclusion -- References -- REM and NREM Sleep Mentation -- I. Introduction -- II. Dreams in REM and NREM Sleep -- III. Neurobiologic Correlates of REM and NREM Sleep That AreConsistent with REM and NREM Sleep Processing Specializations -- IV. Specializations in Emotional Processing -- V. REM-NREM Interactions in Processing of Memories across a SingleNight -- VI. Which (If Any) Elements of REM or NREM Sleep Dream Content AreCorrelated with Daytime Mood and Behavioral Variables? -- VII. Summary -- VIII. Significance -- Acknowledgments -- References -- Neuroimaging of Dreaming: State of the Art and Limitations -- I. Introduction -- II. Necessity of and Difficulties in the Assessment of Dream Reports -- III. Basic Assumptions -- IV. Current Data -- V. Conclusions -- References -- Memory Consolidation, The Diurnal Rhythm of Cortisol, andThe Nature of Dreams: A New Hypothesis -- I. Memory Consolidation, the Diurnal Rhythm of Cortisol, and theFormal Features of Dreaming: A New Hypothesis -- II. Sleep and Memory: The Case for Consolidation. , III. Cortisol's Impact on Memory During Wakefulness -- IV. A Clinical View of Memory Under Stress -- V. Tying It All Together: Toward a New Hypothesis of Dreaming -- VI. The Emotional Nature of Dreams -- VII. Concluding Remarks -- References -- Characteristics and Contents of Dreams -- I. Introduction -- II. Definitions and Methodological Issues -- III. Dream Content Analysis -- IV. Phenomenology of Dreams -- V. Factors Influencing Dream Content -- VI. The "Continuity Hypothesis" of Dreaming -- VII. Dreams and Psychopathology -- VIII. Dreams and Sleep Disorders -- IX. Effect of Dreams on Waking Life -- X. Conclusion and Future Directions -- References -- Trait and Neurobiological Correlates of Individual Differencesin Dream Recall and Dream Content -- I. Individual Differences in DRF -- II. Individual Differences in Dream Content -- III. Neurobiology of Individual Difference Variables Relevant to Dreaming -- IV. Conclusions -- References -- Consciousness in Dreams -- I. Introduction -- II. How Does Dream Consciousness Come About? -- III. What Characterizes Dream Consciousness? -- IV. Characteristics of Dreams -- V. Dream Consciousness and the Dream Body -- VI. How Do Dream Consciousness and Lucidity Differ from WakeConsciousness? -- VII. What We Can Learn from Dream Consciousness -- References -- The Underlying Emotion and the Dream: RelatingDream Imagery to the Dreamer's UnderlyingEmotion can Help Elucidate the Nature of Dreaming -- I. Emotion and Dreaming: Introduction -- II. Dreams and Emotional Arousal: Starting with Trauma and Stress -- III. The Contemporary Theory of Dreaming -- IV. The Clinical Literature versus the Research Literature on Dreams:A Hierarchy of Emotional Intensity -- References -- Dreaming, Handedness, and Sleep Architecture: InterhemisphericMechanisms -- I. Hand Preference: Definition, Measurement, and Neurophysiology. , II. Handedness and Sleep -- III. Summary -- References -- To What Extent Do Neurobiological Sleep-Waking ProcessesSupport Psychoanalysis? -- I. Introduction -- II. Result -- III. What Happens during Sleep -- IV. Conclusion -- Acknowledgments -- References -- The Use of Dreams in Modern Psychotherapy -- I. Theories of Dream Work -- II. Empirical Research on the Demographics of Dream Work inPsychotherapy -- III. Empirical Research on Models of Dream Work -- IV. Empirical Research in Other Areas Related to Dreams andPsychotherapy -- V. Future Directions -- References -- Index -- Contents of Recent Volumes.
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 51 (1988), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Purified tribulin, an endogenous monoamine oxidase (MAO) inhibitor, has been identified by direct probe insertion mass spectrometry as the indole-2,3-dione, isatin. A gas chromatographic-mass spectrometric assay for isatin has been developed and used to measure its relatively high concentrations in unpurified human urine, and in rat heart and brain. Isatin is a known compound with a broad range of biological activity; this is the first report of its presence in the animal body. Isatin is a potent inhibitor of MAO, particularly of MAO B (IC50, 3 μM), and also binds to central benzodiazepine receptors (IC50 against clonazepam, 123 μM).
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  • 5
    ISSN: 1469-8986
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine , Psychology
    Notes: Secretory immunoglobulin A (sIgA) in saliva and cardiovascular reactions to mental arithmetic and cold pressor tasks were recorded in 16 healthy young men on two sessions, 4 weeks apart. Both tasks elicited significant increases in sIgA secretion rate, reflecting increases in both salivary volume and sIgA concentration. Whereas mental arithmetic elicited a mixed pattern of alpha- and beta-adrenergic cardiovascular reactions, the pattern of reactions to cold pressor was predominantly alpha-adrenergic. Task levels of sIgA secretion rate, sIgA concentration, and saliva volume showed moderate to high test–retest reliability (r= .52–.83), although test-retest correlations were less impressive for change scores (r=−.19–.53). The pattern of correlations between change in sIgA secretion rate and cardiovascular reactivity variables was inconsistent.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 45 (1985), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Both alprazolam and triazolam displaced clonazepam (but not Ro 5–4864) from rat brain membranes with high affinity, showing them to act at central but not peripheral benzodiazepine receptors. At 0°C, 10 μMγ-aminobutyric acid (GABA) increased the ability of alprazolam, but not of triazolam, to displace ethyl-β-carboline-3-carboxylate (β-CCE) and Ro 15–1788 from these receptors. At 37°C, GABA increased the affinity of the receptors for both drugs, with a +GABA/–GABA ratio of 1.5 for each in promoting Ro 15–1788 binding displacement. As both triazolam and alprazolam act as anxiolytics in vivo, the results at 37°C would be compatible with the hypothesis that GABA causes an increase in affinity of drugs that act in this way, but the results at 0°C would not be compatible. At 37°C, alprazolam had a higher IC50 for the benzodiazepine receptor than at 0°C, whereas triazolam showed the reverse effect. The relative IC50 values in vitro at 37°C correlated better with the potency in vivo than those obtained at 0°C. At 0°C, both drugs showed Hill plots with slopes of 0.9–1 with β-CCE and Ro 15–1788. At 37°C, the slopes with triazolam were much reduced, indicating that the drug may have a selective action on a subclass of central benzodiazepine receptors. In the studies reported here, alprazolam behaved like other benzodiazepines, whereas triazolam showed several anomalous properties. It would be of interest if these properties could be related either to the drug's use as a hypnotic or to the side effects it sometimes induces.
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  • 7
    ISSN: 1435-1463
    Keywords: Tribulin ; monoamine oxidase inhibition ; benzodiazepine receptor binding inhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A low molecular weight fraction of human urine (〈500 daltons) which both inhibits monoamine oxidase and benzodiazepine binding to central and peripheral receptors has been purified by ethyl acetate extractions, HPLC and thin layer chromatography. This material extracted equally well at acid and basic pH and was insoluble in heptane. It competitively inhibited binding of3H-clonazepam, a central benzodiazepine receptor agonist and, in addition, displaced3H-Ro 5-4864, a specific peripheral benzodiazepine receptor ligand, from its binding sites. It showed no GABA shift with the benzodiazepine receptor antagonist, Ro-15 1788. MAO A and B were inhibited approximately equipotently and the material competitively inhibited tyramine oxidation by rat liver. It was stable on boiling and is unlikely to be a peptide.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 95 (1988), S. 378-380 
    ISSN: 1432-2072
    Keywords: Anxiety ; Monoamine oxidase ; Benzodiazepine receptor ; Endogenous ligand
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Urinary output of an endogenous monoamine oxidase inhibitor and benzodiazepine receptor binding inhibitor (tribulin) was raised in a group of patients with generalised anxiety disorder compared with controls. Tribulin levels remained relatively constant in individual patients over the 6-week period of observation, mean values remaining high even after reduction of anxiety following non-drug behaviour therapy.
    Type of Medium: Electronic Resource
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