Growth hormone-releasing factor enhances sleep in rats and rabbits

Obál, F.; Alföldi, P.; Cady, Alan B.; Johannsen, Lars; Sáry, Gyula; Krueger, James M.

doi:10.1152/ajpregu.1988.255.2.r310

Cited by 60 publications

(58 citation statements)

References 31 publications

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“…Our finding in humans is at variance with the increase of SWA, which followed the suppression of NREMS after octreotide in the rat (Beranek et al, 1997(Beranek et al, , 1999. The decrease of stage 4 sleep after octreotide is in contrast to the increase of SWS after GHRH in humans (Kerkhofs et al, 1993;Marshall et al, 1996;Steiger et al, 1992) and of NREMS in laboratory animals (Obál et al, 1988Ehlers et al, 1986;Nistico et al, 1987;Zhang et al, 1999) and after ghrelin in humans (Weikel et al, 2003) and in mice (Obál et al, 2003). We showed previously that the timing of GHRH administration is a crucial issue.…”

Section: Discussionsupporting

confidence: 55%

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The Somatostatin Analogue Octreotide Impairs Sleep and Decreases EEG Sigma Power in Young Male Subjects

Ziegenbein

Held

Kuenzel

et al. 2003

Neuropsychopharmacol

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The long-acting somatostatin (SRIF) analogue octreotide decreased nonrapid eye movement sleep (NREMS) in the rat. This effect is opposite to the promotion of sleep after growth hormone (GH)-releasing hormone (GHRH) in various species including humans. Therefore, it appears likely that GHRH and SRIF, besides their opposite action on pituitary GH release, interact reciprocally in sleep regulation. In previous studies, SRIF impaired sleep in elderly subjects, although sleep in young men remained unchanged. We hypothesized that octreotide is a useful tool to study the role of SRIF in human sleep regulation. We examined the effect of subcutaneous administration of 0.1 mg octreotide at 2245 on the sleep EEG of seven young male controls (age, mean 7 SD, 22.3 7 3.0 years). In comparison to placebo, octreotide administration prompted decreases of sleep stage 4 during the total night and of rapid eye movement sleep (REMS) density during the first half of the night. Intermittent wakefulness increased during the second half of the night. The spectral analysis of total night NREMS revealed a significant decrease of sigma power. Similar to the effect of the short-acting SRIF in the elderly, the long-acting SRIF analogue octreotide impaired sleep in young healthy subjects. Obviously, the influence of octreotide on sleep is superior to that of short-acting SRIF, which did not affect sleep in young men. We suggest a reciprocal interaction of GHRH and SRIF in sleep regulation.

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Section: Discussionsupporting

confidence: 55%

“…into rabbits (Obál et al, 1988) and rats (Obál et al, 1988;Ehlers et al, 1986;Nistico et al, 1987), intravenously (i.v.) into rats , intraperitoneally (i.p.)…”

Section: Introductionmentioning

confidence: 99%

The Somatostatin Analogue Octreotide Impairs Sleep and Decreases EEG Sigma Power in Young Male Subjects

Ziegenbein

Held

Kuenzel

et al. 2003

Neuropsychopharmacol

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“…In addition, GHRH activates cell proliferation, cell differentiation, and growth of somatotrophs (6)(7)(8). There are many other reported activities of GHRH such as modulation of appetite and feeding behavior, regulation of sleeping (9,10), control of jejunal motility (11), and increase of leptin levels in modest obesity (12).…”

mentioning

confidence: 99%

Discovery of growth hormone-releasing hormones and receptors in nonmammalian vertebrates

Lee¹,

Siu²,

Tam³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

109

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In mammals, growth hormone-releasing hormone (GHRH) is the most important neuroendocrine factor that stimulates the release of growth hormone (GH) from the anterior pituitary. In nonmammalian vertebrates, however, the previously named GHRH-like peptides were unable to demonstrate robust GH-releasing activities. In this article, we provide evidence that these GHRH-like peptides are homologues of mammalian PACAP-related peptides (PRP). Instead, GHRH peptides encoded in cDNAs isolated from goldfish, zebrafish, and African clawed frog were identified. Moreover, receptors specific for these GHRHs were characterized from goldfish and zebrafish. These GHRHs and GHRH receptors (GHRHRs) are phylogenetically and structurally more similar to their mammalian counterparts than the previously named GHRH-like peptides and GHRH-like receptors. Information regarding their chromosomal locations and organization of neighboring genes confirmed that they share the same origins as the mammalian genes. Functionally, the goldfish GHRH dose-dependently activates cAMP production in receptor-transfected CHO cells as well as GH release from goldfish pituitary cells. Tissue distribution studies showed that the goldfish GHRH is expressed almost exclusively in the brain, whereas the goldfish GHRH-R is actively expressed in brain and pituitary. Taken together, these results provide evidence for a previously uncharacterized GHRH-GHRH-R axis in nonmammalian vertebrates. Based on these data, a comprehensive evolutionary scheme for GHRH, PRP-PACAP, and PHI-VIP genes in relation to three rounds of genome duplication early on in vertebrate evolution is proposed. These GHRHs, also found in flounder, Fugu, medaka, stickleback, Tetraodon, and rainbow trout, provide research directions regarding the neuroendocrine control of growth in vertebrates. molecular evolution ͉ genome duplication ͉ pituitary adenylate cyclase-activating polypeptide

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“…Systemic injection of exogenous GHRH promotes nonrapid eye movement sleep (N REMS) in humans (Steiger et al, 1992;Kerkhofs et al, 1993;Marshall et al, 1996) and rats . Intracerebroventricular administration of GHRH increases N REMS and enhances slow-wave activity (SWA) in the electroencephalogram (EEG) during NREMS in rats and rabbits Nistico et al, 1987;Obál et al, 1988). Inhibition of endogenous GHRH using either a peptide antagonist (Obál et al, 1991) or anti-GHRH antibodies (Obál et al, 1992) suppresses spontaneous sleep.…”

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confidence: 99%

Intrapreoptic Microinjection of GHRH or Its Antagonist Alters Sleep in Rats

Zhang¹,

Obál

Zheng

et al. 1999

J. Neurosci.

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Previous reports indicate that growth hormone-releasing hormone (GHRH) is involved in sleep regulation. The site of action mediating the nonrapid eye movement sleep (NREMS)-promoting effects of GHRH is not known, but it is independent from the pituitary. GHRH (0.001, 0.01, and 0.1 nmol/kg) or a competitive antagonist of GHRH (0.003, 0.3, and 14 nmol/kg) was microinjected into the preoptic area, and the sleep-wake activity was recorded for 23 hr after injection in rats. GHRH elicited dosedependent increases in the duration and in the intensity of NREMS compared with that in control records after intrapreoptic injection of physiological saline. The antagonist decreased the duration and intensity of NREMS and prolonged sleep latency. Consistent alterations in rapid eye movement sleep (REMS) and in brain temperature were not found. The GHRH antagonist also attenuated the enhancements in NREMS elicited by 3 hr of sleep deprivation. Histological verification of the injection sites showed that the majority of the effective injections were in the preoptic area and the diagonal band of Broca. The results indicate that the preoptic area mediates the sleeppromoting activity of GHRH.

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Growth hormone-releasing factor enhances sleep in rats and rabbits

Cited by 60 publications

References 31 publications

The Somatostatin Analogue Octreotide Impairs Sleep and Decreases EEG Sigma Power in Young Male Subjects

The Somatostatin Analogue Octreotide Impairs Sleep and Decreases EEG Sigma Power in Young Male Subjects

Discovery of growth hormone-releasing hormones and receptors in nonmammalian vertebrates

Intrapreoptic Microinjection of GHRH or Its Antagonist Alters Sleep in Rats

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