Growth hormone-releasing hormone antibodies suppress sleep and prevent enhancement of sleep after sleep deprivation

Obál, F.; Payne, L. E.; Opp, Mark R.; Alföldi, P.; Kapás, Levente; Krueger, James M.

doi:10.1152/ajpregu.1992.263.5.r1078

Cited by 42 publications

(38 citation statements)

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“…Only a few factors are known to specifically affect SWA homeostasis, most notably growth hormone-releasing hormone (GHRH), interleukin-1␤ (IL-1␤), and adenosine. Interference with the GHRH system or with IL-1␤ expression reduces the SWA response (Obal et al, 1992;Zhang et al, 1999;Yasuda et al, 2005). However, NA depletion is unlikely to act through the GHRH system, because DSP-4 lesions spare the hypothalamic regions where GHRH-synthesizing neurons are located.…”

Section: Discussionmentioning

confidence: 99%

Locus Ceruleus Control of Slow-Wave Homeostasis

Cirelli¹,

Huber²,

Gopalakrishnan³

et al. 2005

J. Neurosci.

104

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Sleep intensity is regulated by the duration of previous wakefulness, suggesting that waking results in the progressive accumulation of sleep need (Borbély and Achermann, 2000). In mammals, sleep intensity is reflected by slow-wave activity (SWA) in the nonrapid eye movement (NREM) sleep electroencephalogram, which increases in proportion to the time spent awake. However, the mechanisms responsible for the increase of NREM SWA after wakefulness remain unclear. According to a recent hypothesis (Tononi and Cirelli, 2003), the increase in SWA occurs because during wakefulness, many cortical circuits undergo synaptic potentiation, as evidenced by the widespread induction of long-term potentiation (LTP)-related genes in the brain of awake animals. A direct prediction of this hypothesis is that manipulations interfering with the induction of LTP-related genes should result in a blunted SWA response.Here, we examined SWA response in rats in which cortical norepinephrine (NA) was depleted, a manipulation that greatly reduces the induction of LTP-related genes during wakefulness (Cirelli and Tononi, 2004). We found that the homeostatic response of the lower-range SWA was markedly and specifically reduced after NA depletion. These data suggest that the wake-dependent accumulation of sleep need is causally related to cellular changes dependent on NA release, such as the induction of LTP-related genes, and support the hypothesis that sleep SWA homeostasis may be related to synaptic potentiation during wakefulness.

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Section: Discussionmentioning

confidence: 99%

Locus Ceruleus Control of Slow-Wave Homeostasis

Cirelli¹,

Huber²,

Gopalakrishnan³

et al. 2005

J. Neurosci.

104

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show abstract

“…GHRH was found, whereas it was weaker than that in young men . In various animal models of reduced GHRH activity NREMS is decreased, as after the suppression of endogenous GHRH by GHRH antibodies (Obál et al, 1991), GHRH antagonists (Obál et al, 1992), in mutant dwarf rats , in dwarf mice with GHRH receptor deficiencies (Obál et al, 2003), and in transgenic mice with decreased GHRH production (Zhang et al, 1996). The diurnal variation of GHRH mRNA levels (Bredow et al, 1996) and GHRH contents in the rat hypothalamus suggests distinct synthesis and release of GHRH, when the peak of NREMS occurs during the first portion of the rest period.…”

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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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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“…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. Blockade of endogenous GHRH by means of immunoneutralization prevents the enhanced recovery sleep after short-term sleep deprivation (Obál et al, 1992).…”

mentioning

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 hormone antibodies suppress sleep and prevent enhancement of sleep after sleep deprivation

Cited by 42 publications

References 0 publications

Locus Ceruleus Control of Slow-Wave Homeostasis

Locus Ceruleus Control of Slow-Wave Homeostasis

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

Intrapreoptic Microinjection of GHRH or Its Antagonist Alters Sleep in Rats

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