The 5-HT1A agonist ipsapirone enhances EEG slow wave activity in human sleep and produces a power spectrum similar to 5-HT2 blockade

Seifritz, Erich; Moore, Polly; Trachsel, L.; Bhatti, Tahir; Stahl, Stephen M.; Gillin, J. Christian

doi:10.1016/0304-3940(96)12607-0

Cited by 37 publications

(20 citation statements)

References 27 publications

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“…Similar changes had been reported for the less selective 5-HT 2 antagonists ritanserin and seganserin (Idzikowski et al 1986;Declerck et al 1987;Borbély et al 1988;Dijk et al 1989). In previous studies, also a 10-mg dose of the 5-HT 1A agonist ipsapirone enhanced SWA in the first two hours of NREMS (Seifritz et al 1996), yet did not increase SWS (Gillin et al 1994. The effects of ipsapirone on EEG power spectra in NREMS were remarkably similar to those induced by seganserin (Seifritz et al 1996).…”

Section: Discussionsupporting

confidence: 80%

“…In previous studies, also a 10-mg dose of the 5-HT 1A agonist ipsapirone enhanced SWA in the first two hours of NREMS (Seifritz et al 1996), yet did not increase SWS (Gillin et al 1994. The effects of ipsapirone on EEG power spectra in NREMS were remarkably similar to those induced by seganserin (Seifritz et al 1996). These results and single unit recordings (Ashby et al 1994) support the notion that inhibitory 5-HT 1A receptors and excitatory 5-HT 2 receptors mediate opposite changes.…”

Section: Discussionsupporting

confidence: 70%

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Serotonin-2 Receptors and Human Sleep Effect of a Selective Antagonist on EEG Power Spectra

Landolt

Meier

Burgess

et al. 1999

Neuropsychopharmacology

102

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To investigate the effect on the sleep EEG, a 1-mg oral dose of SR 46349B, a novel 5-HTThe pivotal role of serotonin (5-hydroxytryptamine, 5-HT) in sleep regulation has been the mainstay of the monoamine theory of sleep (Jouvet 1972). Although the views about the functions of this neurotransmitter have evolved, there is little doubt about its involvement in sleep mechanisms (McCormick 1992). Serotonergic neurons of the nucleus raphe dorsalis are most active during wakefulness and have been proposed to participate in the build-up of sleep propensity (Adrien 1995). Animal studies revealed that these neurons decrease firing upon transition from wakefulness to nonREM sleep (NREMS), and become quiescent during REM sleep (REMS). Thus, deactivation of the serotonergic system may facilitate the production of NREMS and REMS (Adrien 1995). One of the complexities in accounting for the actions of 5-HT is the large number of different receptors and receptor subtypes. 5-HT receptors are classified into four distinct classes, comprising seven fully characterized functional receptor subtypes and several recombinant receptors (Hoyer and Martin 1996). While the involvement of three main classes (i.e., 5-HT 1 , 5-HT 2 , and 5-HT 3 receptors) in the regulation of sleep and wakefulness has been studied, it is the postsynaptic 5-HT 1A receptor that seems to mediate the inhibition of REMS and the promotion of wakefulness, whereas activation of the 5-HT 2 receptor may exert a tonic inhibition of slow wave sleep (SWS) (see Adrien 1995 for review). In relation to sleep homeostasis, the latter is of particular interest because 5-HT 2 antagonists were shown to increase the amount of SWS and to enhance EEG slow-

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Section: Discussionsupporting

confidence: 80%

Section: Discussionsupporting

confidence: 70%

Serotonin-2 Receptors and Human Sleep Effect of a Selective Antagonist on EEG Power Spectra

Landolt

Meier

Burgess

et al. 1999

Neuropsychopharmacology

102

View full text Add to dashboard Cite

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“…The changes of sleep architecture and qEEG in the delta and theta range in the present study are in accordance with these reports. Similar effects were observed after selective stimulation of 5-HT1 receptors with ipsapirone (Seifritz et al, 1996). The enhancement of serotoninergic neurotransmission resulting from 5-HT2 blockade by mirtazapine is specifically mediated via 5-HT1 receptors (Fawcett and Barkin, 1998).…”

Section: Discussionsupporting

confidence: 54%

Changes of Sleep Architecture, Spectral Composition of Sleep EEG, the Nocturnal Secretion of Cortisol, ACTH, GH, Prolactin, Melatonin, Ghrelin, and Leptin, and the DEX-CRH Test in Depressed Patients during Treatment with Mirtazapine

Schmid

Wichniak

Uhr

et al. 2005

Neuropsychopharmacol

146

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The noradrenergic and specific serotoninergic antidepressant mirtazapine improves sleep, modulates hormone secretion including blunting of hypothalamic-pituitary-adrenocortical (HPA) activity, and may prompt increased appetite and weight gain. The simultaneous investigation of sleep electroencephalogram (EEG) and hormone secretion during antidepressive treatment helps to further elucidate these effects. We examined sleep EEG (for later conventional and quantitative analyses) and the nocturnal concentrations of cortisol, adrenocorticotropin (ACTH), growth hormone (GH), prolactin, melatonin and the key factors of energy balance, ghrelin, and leptin before and after 28 days of treatment of depressed patients (seven women, three men, mean age 39.974.2 years) with mirtazapine. In addition, a sleep EEG was recorded at day 2 and the dexamethasone-corticotropin-releasing hormone (DEX-CRH) test was performed to assess HPA activity at days À3 and 26. Psychometry and mirtazapine plasma concentrations were measured weekly. Already at day 2, sleep continuity was improved. This effect persisted at day 28, when slow-wave sleep, low-delta, theta and alpha activity, leptin and (0300-0700) melatonin increased, and cortisol and ghrelin decreased. ACTH and prolactin remained unchanged. The first two specimens of GH collected after the start of quantitative EEG analysis were reduced at day 28. The DEX-CRH test showed, at day 26, a blunting of the overshoot of ACTH and cortisol found at day À3. The Hamilton Depression score decreased from 32.177.3 to 15.576.7 between days À1 and 28. A weight gain of approximately 3 kg was observed. This unique profile of changes is compatible with the action of mirtazapine at 5-HT-2 receptors, at presynaptic adrenergic alpha 2 receptors, at the HPA system, and on ghrelin and leptin.

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“…Alternatively, electroencephalography (EEG) recordings have shown that the administration of 5-HT 1A receptor agonists causes a negative shift of the EEG frequency spectrum. This has been demonstrated with ipsapirone during sleep (Seifritz et al 1996) and buspirone in awake subjects (Anderer et al 1993;McAllister-Williams et al 1997). Buspirone administration to rats has a similar effect that is mirrored by the more selective 5-HT 1A agonist 8-OH-DPAT, but not a dopamine D 2 antagonist (Bogdanov and Bogdanov 1994).…”

Section: Introductionmentioning

confidence: 79%

EEG effects of buspirone and pindolol: a method of examining 5-HT1A receptor function in humans

McAllister-Williams

Massey

2003

Psychopharmacology

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The data obtained are consistent with the EEG effects of buspirone and pindolol being mediated by somatodendritic 5-HT(1A) receptors, in contrast to the neuroendocrine response, which is known to be mediated by postsynaptic receptors. The development of this novel method of assessing somatodendritic 5-HT(1A) receptors in humans is a potentially important advance which may allow the testing of hypotheses of its involvement in depression and response to antidepressants.

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The 5-HT1A agonist ipsapirone enhances EEG slow wave activity in human sleep and produces a power spectrum similar to 5-HT2 blockade

Cited by 37 publications

References 27 publications

Serotonin-2 Receptors and Human Sleep Effect of a Selective Antagonist on EEG Power Spectra

Serotonin-2 Receptors and Human Sleep Effect of a Selective Antagonist on EEG Power Spectra

Changes of Sleep Architecture, Spectral Composition of Sleep EEG, the Nocturnal Secretion of Cortisol, ACTH, GH, Prolactin, Melatonin, Ghrelin, and Leptin, and the DEX-CRH Test in Depressed Patients during Treatment with Mirtazapine

EEG effects of buspirone and pindolol: a method of examining 5-HT1A receptor function in humans

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