Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Extremely small amounts (10(-4) pg) of synthetic arginine vasotocin (AVT) injected into the pineal recess of unanesthetized cats induced a continuous NREM sleep for about 60 minute and completely suppressed REM sleep for about 5 hours. The reappearance of the REM sleep following AVT administration occurred with a marked rebound, lasting for more than one hour. Since neither vasopressin nor oxytocin, at the same doses, were able to affect significantly the REM sleep, it is concluded that AVT is specifically involved in the modulation and/or circadian organization of the REM sleep.
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PMID:REM sleep rebound after its suppression by vasotocin in cats. 368 44

This study is an investigation of the central effects of vasopressin in man, as this hormone proved able to modify learning processes in animals and was applied successfully to post-traumatic, amnesic patients. Electrophysiological techniques were used to assess the effects of lysine-vasopressin (LVP) given by nasal spray (7 and 14 IU) on night sleep pattern (12 subjects), auditory evoked potentials (AEP; 26 subjects), and contingent negative variation (CNV; 26 subjects). Night sleep EEG was not modified to a great extent: in particular REM sleep did not undergo any change after LVP. Nor were AEPs modified, either in the 6-hour period following drug administration or 1 week after; CNV, however, reacted in a significant manner 6 h after drug intake, and the modifications were still present after 1 week. LVP did not affect CNV amplitude itself but its evolution through time, as CNV habituation was prevented. Such effects are discussed with regard to the neurochemical mechanisms of vasopressin action and CNV genesis.
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PMID:Action of lysine-vasopressin on human electroencephalographic activity. Night sleep pattern, auditory evoked potential, contingent negative variation. 713 74

The intention of this review is to summarize the current knowledge on the bidirectional interaction between sleep EEG and the secretion of corticotropin (ACTH) and cortisol. The administration of various hypothalamic-pituitary- adrenocortical (HPA) hormones and their antagonists exerts specific sleep-EEG changes in several species including humans. It is well documented that corticotropin releasing hormone (CRH) impairs sleep and enhances vigilance. In addition, it may promote REM sleep. Changes in the growth hormone-releasing hormone (GHRH):CRH ratio in favour of CRH appear to contribute to shallow sleep, elevated cortisol levels and blunted GH in depression and ageing. On the other hand, in women GHRH appears to exert CRH-like effects on sleep. Acute cortisol administration increases slow-wave sleep (SWS) and GH, probably due to feedback inhibition of CRH, and inhibits REM sleep. With the mixed glucocorticoid and progesterone receptor antagonist mifepriston sleep is disrupted. Subchronic administration of the glucocorticoid agonist methylprednisolone desinhibited REM sleep. A synergism of elevated CRH and cortisol activity may contribute to REM disinhibition during depression. Also ACTH and vasopressin modulate sleep specifically but their physiological role remains unclear. For example acute icv vasopressin enhances wakefulness in rats, whereas its long-term administration increases SWS in the elderly. In various studies the interaction of sleep EEG and HPA hormones has been investigated at the baseline, after manipulation of sleep-wake behaviour and after environmental changes. Most studies agree that the circadian pattern of cortisol is relatively independent from sleep and environmental influences. Some data suggest a major effect of light on cortisol secretion. Sleeping is widely associated with blunting and awakenings are linked with increases of HPA hormones.
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PMID:Sleep and the hypothalamo-pituitary-adrenocortical system. 1253 Nov 48

In different species, rapid eye movement sleep (REMS) is characterized by a thermoregulatory impairment. It has been postulated that this impairment depends on a general insufficiency in the hypothalamic integration of autonomic function. This study aims to test this hypothesis by assessing the hypothalamic regulation of body fluid osmolality during the different wake-sleep states in the rat. Arginine-vasopressin (AVP) plasma levels were determined following intracerebroventricular (ICV) infusions of artificial cerebrospinal fluid (aCSF), either isotonic or made hypertonic by the addition of NaCl at three different concentrations (125, 250 and 500 mM). Animals were implanted with a cannula within a lateral cerebral ventricle for ICV infusions and with electrodes for the recording of the electroencephalogram. ICV infusions were made in different animals during Wake, REMS or non-REM sleep (NREMS). The results show that ICV infusion of hypertonic aCSF during REMS induced an increase in AVP plasma levels that was not different from that observed during either Wake or NREMS. These results suggest that the thermoregulatory impairment that characterizes REMS does not depend on a general impairment in the hypothalamic control of body homeostasis.
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PMID:Hypothalamic osmoregulation is maintained across the wake-sleep cycle in the rat. 2037 48

Thalidomide exerts its teratogenic and immunomodulatory effects by binding to cereblon (CRBN) and thereby inhibiting/modifying the CRBN-mediated ubiquitination pathway consisting of the Cullin4-DDB1-ROC1 E3 ligase complex. The mechanism of thalidomide's classical hypnotic effect remains largely unexplored, however. Here we examined whether CRBN is involved in the hypnotic effect of thalidomide by generating mice harboring a thalidomide-resistant mutant allele of Crbn (Crbn YW/AA knock-in mice). Thalidomide increased non-REM sleep time in Crbn YW/AA knock-in homozygotes and heterozygotes to a similar degree as seen in wild-type littermates. Thalidomide similarly depressed excitatory synaptic transmission in the cortical slices obtained from wild-type and Crbn YW/AA homozygous knock-in mice without affecting GABAergic inhibition. Thalidomide induced Fos expression in vasopressin-containing neurons of the supraoptic nucleus and reduced Fos expression in the tuberomammillary nuclei. Thus, thalidomide's hypnotic effect seems to share some downstream mechanisms with general anesthetics and GABAA-activating sedatives but does not involve the teratogenic CRBN-mediated ubiquitin/proteasome pathway.
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PMID:Hypnotic effect of thalidomide is independent of teratogenic ubiquitin/proteasome pathway. 3284 52