Intrapreoptic Microinjection of GHRH or Its Antagonist Alters Sleep in Rats

Zhang, Jianyi; Obál, F.; Zheng, Tong; Fang, Jidong; Taishi, Ping; Krueger, James M.

doi:10.1523/jneurosci.19-06-02187.1999

Cited by 90 publications

(61 citation statements)

References 50 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%

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%

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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“…However, a similar time-of-day-dependent reduction in duration of spontaneous NREMS occurs in mice lacking the TNF 55 kD soluble receptor (Fang et al, 1997). While EEG SWA activity during NREMS is in part regulated independently from duration of NREMS, the two parameters often covary with each other (Fang et al, 1999). For instance, after sleep loss both are enhanced (Pappenheimer et al, 1975).…”

Section: Discussionmentioning

confidence: 97%

“…Recordings began at light onset (0900 h). The vigilance states NREMS, rapid eye movement sleep (REMS) and wake were determined off line in 10 sec epochs using criteria published previously (Zhang et al, 1999). On the first day, the EEG baseline was recorded and on the following day microinjections were made on each side of the brain.…”

Section: Recording and Analyses Of Eeg Delta Activitymentioning

confidence: 99%

TNFα siRNA reduces brain TNF and EEG delta wave activity in rats

et al. 2007

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Tumor necrosis factor alpha (TNFα) is a pleiotropic cytokine with several CNS physiological and pathophysiological actions including sleep, memory, thermal and appetite regulation. Short interfering RNAs (siRNA) targeting TNFα were incubated with cortical cell cultures and microinjected into the primary somatosensory cortex (SSctx) of rats. The TNFα siRNA treatment specifically reduced TNFα mRNA by 45% in vitro without affecting interleukin-6 or gluR1-4 mRNA levels. In vivo the TNFα siRNAα reduced TNFα mRNA, interleukin-6 mRNA and gluR1 mRNA levels compared to treatment with a scrambled control siRNA. After in vivo microinjection, the density of TNFα-immunoreactive cells in layer V of the SSctx was also reduced. Electroencephalogram (EEG) delta wave power was decreased on days 2 and 3 on the side of the brain that received the TNFα siRNA microinjection relative to the side receiving the control siRNA. These findings support the hypothesis that TNFα siRNA attenuates TNFα mRNA and TNFα protein in the rat cortex and that those reductions reduce cortical EEG delta power. Results also are consistent with the notion that TNFα is involved in CNS physiology including sleep regulation.

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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.

106

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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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Intrapreoptic Microinjection of GHRH or Its Antagonist Alters Sleep in Rats

Cited by 90 publications

References 50 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

TNFα siRNA reduces brain TNF and EEG delta wave activity in rats

Locus Ceruleus Control of Slow-Wave Homeostasis

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