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Chapter 45. Neurobiology of Mood Disorders

Charles F. Gillespie, M.D., Ph.D.; Steven J. Garlow, M.D., Ph.D.; Elisabeth B. Binder, M.D., Ph.D.; Alan F. Schatzberg, M.D.; Charles B. Nemeroff, M.D., Ph.D.
DOI: 10.1176/appi.books.9781585623860.421690

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Excerpt

The search for the biological substrates of affective disorders spans many centuries. Indeed, Hippocrates (460–357 b.c.) speculated that melancholia emerged when environmental conditions, such as the alignment of the planets, caused the spleen to secrete black bile, which then darkened the mood. During the next 2,000 years, few significant contributions to our understanding of mood disorders emerged until Robert Burton's Anatomy of Melancholy (1621). Positing that depressed people often "are born of melancholy parents," Burton anticipated the genetic underpinnings of melancholia as well as other factors in the pathogenesis of depression, including alcohol, diet, and biological rhythms. Through his careful longitudinal observations, Emil Kraepelin (1856–1926) was subsequently able to detect a genetic contribution to manic-depressive illness. Kraepelin also hypothesized that other constitutional factors resulted in specific brain abnormalities in manic-depressive patients, although postmortem tissue studies were unrevealing.

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FIGURE 45–1. Stress–diathesis model of depression.
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TABLE 45–1. Alterations in hypothalamic-pituitary-adrenal (HPA) axis activity in unipolar depression
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TABLE 45–2. Alterations in hypothalamic-pituitary-adrenal (HPA) axis activity in bipolar disorder
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TABLE 45–3. Alterations in hypothalamic-pituitary-thyroid (HPT) axis activity in unipolar depression
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TABLE 45–4. Grades of hypothyroidism
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TABLE 45–5. Alterations in hypothalamic-pituitary-thyroid (HPT) axis activity in bipolar disorder
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TABLE 45–6. Alterations in hypothalamic–growth hormone axis activity in depression
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TABLE 45–7. Alterations of the hypothalamic-pituitary-gonadal axis in depression
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TABLE 45–8. Alterations in the serotonergic system in depression
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TABLE 45–9. Alterations in the noradrenergic system in depression
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TABLE 45–10. Alterations in the dopaminergic system in depression
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TABLE 45–11. Alterations of monoamine oxidase (MAO) activity in depression
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TABLE 45–12. Alterations of the glutamatergic system in depression and bipolar disorder
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TABLE 45–13. Alterations of the GABAergic system in depression
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TABLE 45–14. Alterations of the brain-derived neurotrophic factor system in depression
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TABLE 45–15. Abnormalities of the frontal and prefrontal cortex in unipolar depression by neuroimaging
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TABLE 45–16. Abnormalities of the frontal and prefrontal cortex in bipolar disorder by neuroimaging
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TABLE 45–17. Abnormalities of the subgenual cingulate in depression by neuroimaging
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TABLE 45–18. Abnormalities of the hippocampus in depression by neuroimaging
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TABLE 45–19. Abnormalities of the basal ganglia in unipolar depression by neuroimaging
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TABLE 45–20. Abnormalities of the basal ganglia in bipolar disorder by neuroimaging
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TABLE 45–21. Abnormalities of the amygdala in unipolar depression and bipolar disorder by neuroimaging
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TABLE 45–22. Abnormalities of the thalamus in unipolar depression and bipolar disorder by neuroimaging
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TABLE 45–23. Abnormalities of the pituitary in unipolar depression and bipolar disorder by neuroimaging
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TABLE 45–24. Inflammation and depression
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TABLE 45–25. Genetics and mood disorders

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Sample questions:
1.
The dexamethasone suppression test (DST) was one of the first endocrine challenge tests to be studied in psychiatric patients. Meta-analyses of DST findings have revealed which of the following?
2.
Alterations of the hypothalamic-pituitary-adrenal (HPA) axis have been documented in patients with bipolar disorder. Increased HPA axis activity has been associated with which of the following bipolar subtypes?
3.
Various abnormalities suggestive of dysregulation of the hypothalamic-pituitary-thyroid (HPT) axis have been reported in patients with unipolar depression. Which of the following is not a consistent finding in studies of depressed patients?
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