Central administration of the somatostatin analog  octreotide induces captopril-insensitive sleep responses

Beranek, L.; Hajdu, I.; Gardi, János; Taishi, Ping; Obál, F.; Krueger, James M.

doi:10.1152/ajpregu.1999.277.5.r1297

Cited by 33 publications

(46 citation statements)

References 39 publications

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“…The decrease of stage 4 sleep in our study resembles the decrease of NREMS after SRIF (Rezek et al, 1976) and after octreotide (Beranek et al, 1997(Beranek et al, , 1999 in the rat. Furthermore, wakefulness increased during the second half of the night.…”

Section: Discussionsupporting

confidence: 79%

“…These observations point to a long-lasting effect of the substance on sleep-EEG. 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).…”

Section: Discussionsupporting

confidence: 44%

“…After subcutaneous (s.c.) and after i.c.v. administration of octreotide, NREMS was suppressed dose dependently in rats (Beranek et al, 1997(Beranek et al, , 1999). This effect was followed by distinct increases of EEG slow-wave activity during NREMS 2-3 h after administration.…”

Section: Introductionmentioning

confidence: 91%

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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: 79%

Section: Discussionsupporting

confidence: 44%

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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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“…Our results agree with this and other data (2,20), showing that somatostatin analog OCT inhibits sleep (both NREM sleep and REM sleep). Somatostatin inhibits the synthesis and release of GHRH (24,62).…”

Section: Effect Of Somatostatin Analog Octreotidesupporting

confidence: 94%

“…Central administration of OCT also results in a drinking response, and rats display other behavioral changes (such as feeding, grooming, and exploration), parallel with the reduction of sleep time (2). OCT-induced drinking, vasopressin secretion, and rises in blood pressure are attributed to a stimulation of ANG II release (21).…”

Section: Effect Of Somatostatin Analog Octreotidementioning

confidence: 99%

Growth hormone-releasing hormone activates sleep regulatory neurons of the rat preoptic hypothalamus

Péterfi

McGinty

Sarai

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Peterfi Z, McGinty D, Sarai E, Szymusiak R. Growth hormone-releasing hormone activates sleep regulatory neurons of the rat preoptic hypothalamus. Am J Physiol Regul Integr Comp Physiol 298: R147-R156, 2010. First published November 4, 2009 doi:10.1152/ajpregu.00494.2009.-We examined whether growth hormone-releasing hormone (GHRH) may promote non-rapid eye movement (NREM) sleep via activation of GABAergic neurons in the preoptic area. Male Sprague-Dawley rats were implanted with EEG, EMG electrodes and a unilateral intracerebroventricular cannula. Groups of rats received injections (3 l icv) with gonadotropinreleasing hormone (GHRH) (0.1 nmol/100 g body wt) or equal volume of physiological saline at the onset of the dark period and were permitted spontaneous sleep for 90 min. Separate groups of rats were sleep deprived by gentle handling for 90 min, beginning at the time of GHRH or saline injection, at the onset of the dark period. Other groups of rats received intracerebroventricular octreotide (somatostatin analog OCT) injections, intracerebroventricular injection of one of two doses of competitive GHRH antagonist, or intracerebroventricular saline injection at light onset and were then permitted 90 min spontaneous sleep-waking. Rats were killed immediately after the 90-min sleep/wake monitoring period. Brain tissue was processed for immunohistochemistry for c-Fos protein and glutamic acid decarboxylase (GAD). Single c-Fos and dual Fos-GAD cell counts were determined in the median preoptic nucleus (MnPN), and in the core and the extended parts of the ventrolateral preoptic nucleus (cVLPO and exVLPO). Intracerebroventricular GHRH elicited a significant increase in NREM sleep amount. Double-labeled FosϩGAD cell counts were significantly elevated after GHRH injection in the MnPN and VLPO in both undisturbed and sleep-deprived groups. OCT and GHRH antagonist significantly decreased NREM sleep amount compared with control rats. OCT injection increased single c-Fos-labeled cell counts in the MnPN, but not in the VLPO. Double-labeled cell counts were significantly reduced after OCT and the high dose of GHRH antagonist injection in all areas examined. These findings identify GABAergic neurons in the MnPN and VLPO as potential targets of the sleep-regulatory actions of GHRH. preoptic area; growth hormone-releasing hormone; somatostatin; octreotide; median preoptic nucleus; ventrolateral preoptic nucleus GROWTH HORMONE-RELEASING HORMONE (GHRH) is the main stimulatory neuropeptide that regulates growth hormone (GH) release by the pituitary. Exogenous GHRH stimulates sleep, especially, non-rapid eye movement (NREM) sleep (reviewed in Ref. 39). Intracerebroventricular (icv) administration of GHRH increases NREM sleep and enhances EEG slow-wave activity (SWA) in the neocortical EEG during NREM sleep in rats and rabbits (11,37,38). Intravenous administration of GHRH promotes sleep and EEG SWA in humans (25,33,54).In humans, the major daily pulse in GH release occurs early in the nocturnal sleep period, coinciding with the o...

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Neurochemical characterization of receptor‐expressing cell populations by in vivo agonist‐induced internalization: Insights from the somatostatin sst2A receptor

Csaba

Simon

Helboe

et al. 2002

J of Comparative Neurology

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Characterization of both neurochemical phenotype of G protein-coupled receptor (GPCR)-expressing cells and receptor compartmentalization is a prerequisite for the elucidation of receptor functions in the central nervous system. However, it is often prevented by the diffuse and homogeneous distribution of receptor immunoreactivity. This is particularly true for the somatostatin (SRIF) sst2A receptor, which is largely distributed in the mammalian brain. By using this receptor as a model, we investigated whether receptor internalization, a biochemical property shared by numerous GPCRs, would reveal sst2A-expressing cell populations in the rat dorsolateral septum (LSD), a region in which SRIF might play an important modulatory role. Thirty minutes to 1 hour after intracerebroventricular injection of the sst2A receptor agonist octreotide, numerous sst2A-immunoreactive neurons and processes became apparent due to intracytoplasmic accumulation of intensely stained granules. Double-immunolabeling experiments with synaptophysin and MAP2 provided evidence that internalized sst2A receptors are predominantly localized in the somatodendritic compartment. Revealing sst2A receptor-expressing cell bodies permitted to analyze their neurotransmitter content. Quantitative analysis demonstrated an extensive overlap (approximately 85%) between SRIF- and sst2A-expressing neuronal populations. Additionally, numerous SRIF-immunoreactive axon-like terminals were found in close apposition with sst2A-positive cell bodies and dendrites. Taken together, these data suggest that the sst2A receptor is predominantly expressed in LSD neurons as a postsynaptic autoreceptor, thus providing novel neuroanatomic clues to elucidate SRIF neurotransmission in this region. More generally, in vivo agonist-induced internalization appears as a rapid and powerful tool for the neurochemical characterization of GPCR-expressing cell populations in the mammalian brain.

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Central administration of the somatostatin analog octreotide induces captopril-insensitive sleep responses

Cited by 33 publications

References 39 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

Growth hormone-releasing hormone activates sleep regulatory neurons of the rat preoptic hypothalamus

Neurochemical characterization of receptor‐expressing cell populations by in vivo agonist‐induced internalization: Insights from the somatostatin sst2A receptor

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