Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917801 (insomnia)
 10,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Somatostatin-like immunoreactivity was measured in the cerebrospinal fluid (CSF) of 85 inpatients with current or recent episodes of major depressive disorders, diagnosed according to Research Diagnostic Criteria (RDC) as assessed with the Schedule for Affective Disorders and Schizophrenia (SADS). Several biopsychiatric tests were run during the same week of investigation. Results indicate low levels of CSF somatostatin to be a state marker for episodes of depression characterized by sad appearance, feelings of tiredness, insomnia, and subjective inability to acknowledge any external precipitants for the depression. CSF somatostatin was negatively related to platelet monoamine oxidase (MAO) activity; MAO activity appeared to account better for the degree of melancholic features than did somatostatin. The ratio between 3-methoxy-4-hydroxyphenylglycol (MHPG) and homovanillic acid (HVA) in CSF also correlated negatively with somatostatin. A positive relationship was noted between CSF xanthine and somatostatin. There was a highly significant curvilinear correlation between CSF somatostatin and serum TSH concentrations, but no correlations between CSF somatostatin and serum GH or prolactin, or with plasma cortisol before or after dexamethasone.
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PMID:Low levels of somatostatin in human CSF mark depressive episodes. 614 88

A bidirectional interaction exists between the electrophysiological and neuroendocrine components of sleep. The first is represented by the nonrapid eye movement sleep (NREMS) and rapid eye movement sleep (REMS) cycles, the latter by distinct patterns of the secretion of various hormones. Certain hormones (neuropeptides and steroids) play a specific role in sleep regulation. Changes in their activity contribute to the pathophysiology of sleep disorders. A reciprocal interaction of the peptides growth hormone-releasing hormone (GHRH) and corticotropin-releasing hormone (CRH) plays a key role in sleep regulation. GHRH promotes growth hormone secretion and, at least in males, NREMS, whereas CRH impairs NREMS, promotes REMS and stimulates the secretion of adrenocorticotropic hormone and cortisol. Changes in the CRH:GHRH ratio in favor of CRH contribute to impaired sleep, elevated cortisol secretion and blunted GH levels during depression and normal aging. However, in women, GHRH exerts CRH-like effects. Galanin, ghrelin and neuropeptide Y are other sleep-promoting peptides, whereas somatostatin impairs sleep. A decline of orexin activity causes narcolepsy. In addition to CRH overactivity, hypercortisolism appears to be involved in the pathophysiology of sleep- electroencephalogram (EEG) changes in depression. Various neuroactive steroids exert specific effects on sleep. The changes of sleep EEG in women after the menopause are related to the decline of estrogen and progesterone. Furthermore, sleep-EEG changes in dwarfism, acromegaly, Addison's disease, Cushing's disease, brain injury, sleep apnea syndrome, primary insomnia, prolactinoma and dementia appear to be related to changes in the activity of peptides and steroids.
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PMID:Roles of peptides and steroids in sleep disorders. 3075 93