Human plasma DSIP decreases at the initiation of sleep at different circadian times

ArticleinPeptides 16(8):1475-81 · February 1995with4 Reads
DOI: 10.1016/0196-9781(95)02027-6 · Source: PubMed
Nocturnal plasma delta sleep-inducing peptide-like immunoreactivity (DSIP-LI) was determined serially in seven healthy male subjects. Time courses during nocturnal sleep (2300-0800 h), nocturnal sleep deprivation (2300-0500 h), and morning recovery sleep (0500-0800 h) after sleep deprivation were compared. A significant decrease in plasma DSIP-LI was found at the transition from wakefulness to sleep in both evening sleep (2300 h) and morning recovery sleep (0500 h). Time courses were accompanied by physiological changes in sleep electroencephalographic slow-wave activity, and in plasma concentrations of cortisol and human growth hormone. No sleep stage specificity was found. It is concluded that DSIP is influenced by the initiation of sleep.
    • "A close correlation between the diurnal rhythm of DSIP-LI and that of body temperature was detected. It was concluded that endogenous elevation of DSIP may be associated with suppression of both SWS and paradoxical sleep (PS), and that the circadian rhythm of DSIP is coupled directly or indirectly to that of body temperature (Friedman et al. 1994b; Schulz et al. 1994; Seifritz et al. 1995; Steiger and Holsboer 1997); (iv) cardiotropic and vasomotor activity (DSIP can normalize blood pressure and myocardial contraction; Schoenenberger 1984; Yehuda et al. 1988; Inoué 1989; Prudchenko et al. 1994; Strekalova 1998); (v) pain, where DSIP can produce an analgesic effect by augmenting met-encephalin binding with opiate receptors (Schoenenberger 1984; Yehuda et al. 1988; Inoué et al. 1990; Prudchenko et al. 1994; Lysenko et al. 1995; Strekalova 1998; Pollard and Pomfrett 2001); (vi) regulation of diurnal and circadian rhythmicity (Friedman et al. 1994b; Schulz et al. 1994; Seifritz et al. 1995 ; Vgontzas et al. 1995) ; ( vii) anti - opioid and anti - alcohol activity ( DSIP can suppress the development of alcohol and opiate dependency this being the basis for DSIP clinical application ; Yukhana - nov et al. 1991 , 1992 ; Soyka and Rothenhaeusler 1997 ; Backmund et al . 1998 ; Hruz et al . "
    [Show abstract] [Hide abstract] ABSTRACT: Delta sleep-inducing peptide (DSIP) was isolated from rabbit cerebral venous blood by Schoenenberger-Monnier group from Basel in 1977 and initially regarded as a candidate sleep-promoting factor. However, the link between DSIP and sleep has never been further characterized, in part because of the lack of isolation of the DSIP gene, protein and possible related receptor. Thus the hypothesis regarding DSIP as a sleep factor is extremely poorly documented and still weak. Although DSIP itself presented a focus of study for a number of researchers, its natural occurrence and biological activity still remains obscure. DSIP structure is different from any other known representative of the various peptide families. In this mini-review we hypothesize the existence of a DSIP-like peptide(s) that is responsible (at least partly) for DSIP-like immunoreactivity and DSIP biological activity. This assumption is based on: (i) a highly specific distribution of DSIP-like immunoreactivity in the neurosecretory hypothalamic nuclei of various vertebrate species that are not particularly relevant for sleep regulation, as revealed by the histochemical studies of the Geneva group (Charnay et al.); (ii) a large spectrum of DSIP biological activity revealed by biochemical and physiological studies in vitro; (iii) significant slow-wave sleep (SWS) promoting activity of certain artificial DSIP structural analogues (but not DSIP itself!) in rabbits and rats revealed by our early studies; and (iv) significant SWS-promoting activity of a naturally occurring dermorphin-decapeptide that is structurally similar to DSIP (in five of the nine positions) and the sleep-suppressing effect of its optical isomer, as revealed in rabbits. Potential future studies are outlined, including natural synthesis and release of this DSIP-like peptide and its role in neuroendocrine regulation.
    Full-text · Article · May 2006
  • [Show abstract] [Hide abstract] ABSTRACT: Results from preclinical studies have validated the participation of neuropeptides in sleep regulation. In recent human and clinical studies it has been shown that peripheral administration of various peptides results in specific changes in the sleep electroencephalogram in humans. Furthermore, it has been demonstrated that certain peptides are common regulators of the electrophysiological and neuroendocrine components of sleep. It is now well established that the balance between the neuropeptides growth hormone-releasing hormone (GHRH) and corticotropin-releasing hormone (CRH) plays a key role in normal and pathological sleep regulation. In young normal subjects, GHRH stimulates slow-wave sleep and growth hormone secretion but inhibits cortisol release, whereas CRH has the opposite effect. During normal aging and during acute depression, the GHRH:CRH ratio is changed in favor of CRH, resulting in disturbances in sleep endocrine activity. In addition to GHRH, galanin, growth hormone-releasing peptide, and neuropeptide Y also promote sleep, unlike ACTH(4-9), which disturbs sleep. In elderly subjects, sleep deteriorates after acute administration of somatostatin but improves after chronic treatment with vasopressin. Vasoactive intestinal polypeptide decelerates the non-rapid eye movement-rapid eye movement cycle and advances the occurrence of the cortisol nadir. The impact of delta sleep-inducing peptide, cholecystokinin, and thyrotropin-releasing hormone on human sleep regulation is not yet clear. This paper reviews recent work investigating the influence of these various neuropeptides on sleep.
    Article · Dec 1997
  • [Show abstract] [Hide abstract] ABSTRACT: Effects of peptides on the central nervous system are presented in two ways so as to provide a cross-listing. In the first table, the peptides are listed alphabetically. In the second table, the central nervous system effects are arranged alphabetically. No longer can there be any doubt that peptides affect the central nervous system, sometimes in several ways.
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