Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When applied centrally to animals, growth hormone-releasing hormone (GHRH) stimulates slow-wave sleep (SWS), whereas somatostatin (SRIF) increases REM sleep. We investigated whether these peptides also affect the sleep EEG in humans when given intravenously by comparing polysomnographically the effects of four boluses of (1) placebo, (2) 50 micrograms GHRH or (3) 50 micrograms SRIF administered at 22.00, 23.00, 24.00 and 1.00 h to 7 male controls. In addition, we collected blood samples through a long catheter every 20 min from 22.00 to 7.00 h and measured plasma cortisol and growth hormone (GH) levels. In comparison with SRIF and placebo, GHRH produced a significant increase in plasma GH concentration throughout the night (mean +/- SD: 10.8 +/- 2.0 ng/ml after GHRH; 3.0 +/- 1.7 ng/ml after SRIF and 3.2 +/- 2.0 ng/ml after placebo). SRIF failed to substantially attenuate the nocturnal GH release. Nocturnal cortisol secretion was blunted after GHRH but remained unaffected by SRIF (61.4 +/- 12.9 ng/ml after placebo; 46.6 +/- 19.7 ng/ml after GHRH and 70.8 +/- 12.6 ng/ml after SRIF). Quantitative sleep EEG staging showed a significant increase in SWS after GHRH administration but no change after SRIF (percent spent in SWS per night: 14.0 +/- 5.6 after placebo, 20.2 +/- 6.6 after GHRH and 15.1 +/- 8.2 after SRIF). Application of SRIF was accompanied by a trend toward increased REM density. The effects of episodic GHRH administration upon SWS, GH and cortisol secretion were opposite to those previously reported for corticotropin-releasing hormone, which supports the view that neuroregulation of human sleep involves an interaction of central GHRH and corticotropin-releasing hormone.
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PMID:Effects of growth hormone-releasing hormone and somatostatin on sleep EEG and nocturnal hormone secretion in male controls. 136 64

This study examined the relationship between aldosterone secretion and sleep stages in conjunction with two aldosterone regulating hormone systems, the renin-angiotensin system (RAS) and adrenocorticotropin (ACTH), and also K+. Nocturnal plasma patterns of aldosterone, plasma renin activity (PRA), ACTH and K+ were established in blood collected at 10-min intervals in two groups of 6 subjects. Both groups underwent two 9 hour overnight-studies, consisting of one control night and one experimental night. The first group was maintained on a low Na diet and the other was given a beta-blocker, atenolol. Polygraphic recordings of sleep were scored according to established criteria. For the control night, REM sleep usually began at peak level or in the descending phase of aldosterone oscillations. As previously described, PRA reflected REM-NREM sleep alteration, levels increased in NREM and decreased during REM sleep. ACTH fluctuations did not oscillate with sleep stages, but levels were very seldom in the ascending phase at REM sleep onset. Plasma K+ remained almost constant throughout the night. The relative importance of the ACTH and the RAS on nocturnal aldosterone secretion and the relationship between aldosterone oscillations and sleep stages remained unclear. Modulating renin levels by either consuming a low Na diet or administration of a beta-blocker enabled this relationship to be clarified. The RAS dominated aldosterone secretion when stimulated by a low sodium diet. Aldosterone oscillations then reflected PRA oscillations with a delay of about 20 min and the relationship of aldosterone to sleep stages was dependent on the relationship of PRA with sleep stages.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nocturnal oscillations of plasma aldosterone in relation to sleep stages. 196 35

We report on the psychometric, polysomnographic, and neuroendocrine status of 12 subjects at high familial risk for psychiatric disorders and of 10 healthy subjects not at high risk. The psychometric measurements in the high-risk probands revealed an accentuated 'stress personality' pattern and an increased neuroticism score. Their all-night EEG sleep tended to be shallower than that of the control subjects (i.e., decreased sleep efficiency, more frequent awakenings, less slow-wave sleep), whereas they did not differ on REM sleep parameters. The challenge of the limbic-hypothalamic-pituitary-adrenocortical system with corticotropin-releasing hormone after pretreatment with dexamethasone yielded no differences in cortisol secretion between the groups. On an intraindividual level, however, all subjects at high risk except one were found to be conspicuous in at least one of the three states examined.
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PMID:Psychometric, polysomnographic, and neuroendocrine measures in subjects at high risk for psychiatric disorders: preliminary results. 207 34

REM sleep deprivation induced by means of the platform technique (72 h) was followed by a period of latency to sleep characterized by a marked excitement in rats. The administration of naloxone at the end of the REM deprivation period reduced this latency to sleep while morphine, beta-endorphin and DADLE prolonged it. The dopamine D1 receptor antagonist SCH 23390 was extremely potent (0.003 mg/kg) to reduce the latency to sleep and the excitement while the D1 agonist SKF 38393 induced an opposite effect. The dopamine D2 receptor antagonist L-sulpiride was inactive up to a dose of 25 mg/kg. These data suggest that hyperactivity of the opioid and dopamine systems (specifically mediated through D1 receptors) is involved in such behaviour.
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PMID:Stress-induced insomnia: opioid-dopamine interactions. 289 86

We compared the nocturnal plasma prolactin (PRL) and beta-endorphin (B-E) concentrations prior to and after sleep deprivation (SD) in eight epileptic patients with complex partial seizures. After the period of SD (1) the mean number of interictal epileptiform discharges and the mean plasma PRL levels showed a significant rise during light non-REM stages of sleep, and (2) mean nocturnal plasma PRL and B-E concentrations showed a moderate rise during the first few hours of sleep, significant only for plasma PRL. In a patient with multiple complex partial seizures during sleep, the levels of plasma PRL and B-E concentrations were closely related to ictal discharges. The data obtained in this stress-free environment suggest a centrally mediated interaction between the release of PRL and B-E, in relation to epileptic discharges.
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PMID:The effect of epileptiform discharges on neurohormonal release in epileptic patients with complex partial seizures. 296 4

Human sleep is characterized by the cyclic occurrence of nonREM and REM periods and by distinct patterns of nocturnal hormone secretion. A host of factors may result in disturbed sleep, including normal aging and depression. In both states, similar changes in sleep-endocrine activity occur, including decreases in slow wave sleep and in growth hormone secretion. Preclinical investigations and studies by our laboratory in young and elderly normal controls and in patients with depression demonstrate that neuropeptides play a key role in sleep regulation. As an example, growth hormone-releasing hormone (GHRH) is a common stimulus of slow wave sleep and growth hormone release, whereas corticotropin-releasing hormone (CRH) exerts opposite effects. We suggest that an imbalance of both peptides in favor of CRH contributes to changes in sleep-endocrine activity during depression and aging.
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PMID:[Physiology and pathophysiology of sleep]. 853 82

Pharmacological challenge paradigms have been useful for elucidating the phenomenology and neurobiology of panic attacks. A drawback of the pharmacological challenge method is that individual differences in baseline arousal and outcome expectancy can lead to different subjective and physiological drug responses. One method for eliminating differences in baseline arousal and expectancy is to perform pharmacological challenges during non-rapid eye movement (non-REM) sleep. In the present study, fourteen healthy male volunteers received caffeine (5 mg/kg) and placebo (normal saline) during non-REM sleep on two successive nights, in a single-blind manner. Caffeine, compared to placebo, was associated with increased arousal, sleep disruption, and elevations in adrenocorticotropic hormone (ACTH) and cortisol. In one subject, caffeine infusion during sleep induced a panic attack. These findings indicate that caffeine leads to increased arousal and hypothalamic-pituitary-adrenal axis (HPA) axis activation in the absence of high baseline anxiety and expectancy bias. Further, they suggest that similar techniques can be employed in patient populations to elucidate the neurobiology of sleep panic attacks.
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PMID:Effects of intravenous caffeine administered to healthy males during sleep. 925 Apr 37

Pituitary hormone secretion is changed by sleep-awake rhythm, which also regulates by the hypothalamo-pituitary axis. The endocrine rhythm is also affected by such factors as aging and environment conditions. Nocturnal secretion of growth hormone is known to be induced by slow-wave sleep. Plasma prolactin levels seem to increase during REM sleep. Serum thyroid stimulating hormone levels increase during the night. Plasma adrenocorticotropin and cortisol levels increase in the early morning and decreased in the night, which are not related to the sleep stage. The sleep-related hormone secretion is not shown in the patients with disordered hypothalamo-pituitary axis. The evaluation of sleep-related changes in pituitary hormone is important to assess the hypothalamo-pituitary function.
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PMID:[Fluctuations of physical function affected by sleep-awake rhythm--endocrine system]. 950 32

A set of data suggests that the thyroid gland plays a role in the bi-directional interaction between the electrophysiological and the endocrine components of sleep, e.g. the nonREM-REM-cycle and the patterns of nocturnal hormone secretion, respectively. In detail thyroid-stimulating hormone (TSH) and thyroxin (T4) show circadian rhythms. A specific relationship was observed between TSH and REM sleep. Blunted TSH levels were found in healthy elderly subjects and, probably due to overactivity of corticotropin-releasing hormone in patients with depression in comparison to young normal controls. Pulsatile administration of thyrotropin-releasing hormone induced a decrease of sleep efficiency and an earlier occurrence of the cortisol rise in normal controls. Slow wave sleep was reduced in patients with hypothyroidism in comparison to normal controls. The sleep EEG normalised after therapy.
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PMID:[Thyroid gland and sleep]. 1052 32

Anxiolytic and sedative effects of neuropeptide Y (NPY) are thought to involve inhibition of corticotropin-releasing hormone (CRH). Enhanced secretion of CRH plays a critical role in the pathophysiology of major depression, characterized by sleep disturbances, anxiety and loss of appetite. We examined for the first time in young men effects of intravenous injections of NPY (4x50 or 100 microg, n = 9 and 11, respectively, at 22.00, 23.00, 24. 00 and 01.00 compared to saline) on the sleep electroencephalogram (EEG; recorded from 23.00 to 07.00) and nocturnal secretion of adrenocorticotrophic hormone (ACTH), cortisol, growth hormone (GH), prolactin and leptin. Repeated measures MANOVA showed that ACTH secretion during the first half of the night was reduced by the lower dose of NPY only (F = 8.7, p<0.05), while cortisol secretion during the second half of the night was reduced regardless of the dose (F = 7.9, p<0.05). Regardless of the dose, NPY enhanced sleep period time and stage 2 sleep (F = 12.8 and 5.4, each p<0.05), and also reduced sleep latency and time awake (F = 4.9 and 4.4, each p<0.05) and modulated REM sleep. In summary, NPY promotes sleep and inhibits the hypothalamo-pituitary-adrenocortical (HPA) axis in humans, pointing to a possible role of NPY agonists for the development of novel treatment strategies for affective disorders.
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PMID:Neuropeptide Y promotes sleep and inhibits ACTH and cortisol release in young men. 1081 63


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