Effects of Growth Hormone-Releasing Hormone and Somatostatin on Sleep EEG and Nocturnal Hormone Secretion in Male Controls

Steiger, Axel; Güldner, J.; Hemmeter, Ulrich; Rothe, B.; Wiedemann, Klaus; Holsboer, Florian

doi:10.1159/000126275

Cited by 197 publications

(126 citation statements)

References 22 publications

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“…SRIF (Frieboes et al, 1997). Since in young subjects sleep remained unchanged after SRIF (Parker et al, 1974;Kupfer et al, 1992;Steiger et al, 1992), we suggest that the longer half-life time of octreotide was the prerequisite to modulate sleep in young subjects in the present study. Interestingly, the administration of octreotide at 2245, relatively short before sleep onset, prompted a decrease of stage 4 sleep throughout the night in our study.…”

Section: Discussionsupporting

confidence: 45%

“…These findings suggest that SRIF inhibits REMS in humans, either by decreasing the amount of rapid eye movements in young subjects or by decreasing the time spent in REMS in the elderly. This observation points again to a GHRH antagonistic action of SRIF, since GHRH increased, besides NREMS and also REMS, in some (Kerkhofs et al, 1993;Marshall et al, 1996) but not all studies (Steiger et al, 1992) in humans and in rats . In contrast, Danguir and co-workers reported increases of REMS after i.c.v.…”

Section: Discussionmentioning

confidence: 78%

“…Similarly, SWS increased after i.v. GHRH in young normal male subjects (Steiger et al, 1992;Kerkhofs et al, 1993;Marshall et al, 1996) and NREMS increased in a large group of healthy and depressed male subjects of a wide age range, whereas sleep was impaired after i.v. GHRH in female subjects (Antonijevic et al, 2000a, b).…”

Section: Introductionmentioning

confidence: 95%

“…Neither continuous (Parker et al, 1974;Kupfer et al, 1992) nor repetitive i.v. administration of SRIF (Steiger et al, 1992) modulated sleep EEG in healthy adults 20-40 years old. However, when the latter protocol was applied in a sample of elderly normal women and men, sleep was impaired (Frieboes et al, 1997).…”

Section: Introductionmentioning

confidence: 97%

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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: 45%

Section: Discussionmentioning

confidence: 78%

Section: Introductionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 97%

See 2 more Smart Citations

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 order to fully understand the effect of the endocrine challenge on delta sleep in PTSD and controls, and address any issues regarding bioavailability of metyrapone, it will be necessary to confirm comparable cortisol suppression across groups by repeated sampling of nocturnal hormone activity during the sleep recordings. In addition, given the known inhibitory effect of CRF on the somatotropic axis (Holsboer et al, 1988;Steiger et al, 1992) and the known relation between delta sleep and growth hormone release (Van Cauter et al, 2000), it will be necessary to measure growth hormone responses in order to understand fully the effect of metyrapone on delta sleep.…”

Section: Discussionmentioning

confidence: 99%

Delta Sleep Response to Metyrapone in Post-Traumatic Stress Disorder

Neylan

Lenoci

Maglione

et al. 2003

Neuropsychopharmacol

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Metyrapone blocks cortisol synthesis, which results in the stimulation of hypothalamic cortiocotropin-releasing factor (CRF) and a reduction in delta sleep. We examined the effect of metyrapone administration on endocrine and sleep measures in male subjects with and without chronic PTSD. We hypothesized that metyrapone would result in a decrease in delta sleep and that the magnitude of this decrease would be correlated with the endocrine response. Finally, we utilized the delta sleep response to metyrapone as an indirect measure of hypothalamic CRF activity and hypothesized that PTSD subjects would have decreased delta sleep at baseline and a greater decrease in delta sleep induced by metyrapone. Three nights of polysomnography were obtained in 24 male subjects with combatrelated PTSD and 18 male combat-exposed normal controls. On day 3, metyrapone was administered during normal waking hours until habitual sleep onset preceding night 3. Endocrine responses to metyrapone were measured in plasma obtained the morning following sleep recordings, the day before and after administration. Repeated measures ANOVAs were conducted to compare the endocrine and sleep response to metyrapone in PTSD and controls. PTSD subjects had significantly less delta sleep as indexed by stages 3 and 4, and total delta integrated amplitude prior to metyrapone administration. There were no differences in premetyrapone cortisol or ACTH levels in PTSD vs controls. PTSD subjects had a significantly decreased ACTH response to metyrapone compared to controls. Metyrapone caused an increase in awakenings and a marked decrease in quantitative measures of delta sleep that was significantly greater in controls compared to PTSD. The decline in delta sleep was significantly associated with the magnitude of increase in both 11-deoxycortisol and ACTH. The results suggest that the delta sleep response to metyrapone is a measure of the brain response to increases in hypothalamic CRF. These data also suggest that the ACTH and sleep EEG response to hypothalamic CRF is decreased in PTSD.

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Immunohistochemical distribution of the somatostatin receptor subtype 5 in the adult rat brain: Predominant expression in the basal forebrain

1999

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Somatostatin exerts its actions by means of a family of G protein–coupled receptors, five of which have so far been cloned. Whereas mRNAs for receptor subtypes sst1–sst4 have been unequivocally localized in the brain, the data concerning the fifth subtype, sst5, are contradictory. Moreover, whereas sst1 and sst2A receptor proteins have been localized by immunohistochemistry, the distribution of sst3–sst5 receptor proteins and/or subtype‐specific binding remains to be determined in the central nervous system. In the present study, we investigated the distribution of immunoreactive sst5 in adult rat brain and pituitary and demonstrated the presence of this receptor protein in the central nervous system by using an affinity‐purified antibody generated against the C‐terminus of the receptor. The specificity of the antibody for sst5 was established by immunoblotting experiments on membranes prepared from cells transfected with cDNA encoding different somatotropin release inhibiting (SRIF) receptor subtypes as well as from anterior pituitary. In both systems, the antibody specifically recognized a band at approximately 50 kDa molecular mass, corresponding well to the reported size of the cloned receptor (48 kDa). Immunofluorescence in COS‐7 cells transfected with individual SRIF receptor subtypes as well as in sections of rat pituitary demonstrated the antibody's applicability to the immunohistochemical detection of sst5 receptors. In rat brain sections, sst5 immunoreactivity was predominantly associated with neuronal perikarya and primary dendrites. Immunolabeling was most prominent in the olfactory tubercle, islands of Calleja, diagonal band of Broca, substantia innominata, and magnocellular preoptic nucleus of the basal forebrain as well as in the reticular nucleus of the thalamus. Other, less intensely labeled areas included the cerebral cortex, hippocampus, amygdala, preoptic area as well as the lateroanterior nucleus of the hypothalamus. The present findings provide the first characterization of the anatomic distribution of sst5 receptors in the rat brain. They demonstrate a prominent expression of these receptors in the basal forebrain, suggesting that they may be involved in the mediation of somatostatin effects on the sleep‐wake cycle through their association with cortically projecting subcortical systems. J. Comp. Neurol. 412:69–82, 1999. © 1999 Wiley‐Liss, Inc.

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Effects of Growth Hormone-Releasing Hormone and Somatostatin on Sleep EEG and Nocturnal Hormone Secretion in Male Controls

Cited by 197 publications

References 22 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

Delta Sleep Response to Metyrapone in Post-Traumatic Stress Disorder

Immunohistochemical distribution of the somatostatin receptor subtype 5 in the adult rat brain: Predominant expression in the basal forebrain

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