Central action of 5-HT3 receptor ligands in the regulation of sleep-wakefulness and raphe neuronal activity in the rat

Adrien, Joëlle; Tissier, Marie-Hélène; Lanfumey, Laurence; Haj‐Dahmane, Samir; Jolas, Thierry; Franc, Bernard; Hamon, Michel

doi:10.1016/0028-3908(92)90183-p

Cited by 34 publications

(11 citation statements)

References 26 publications

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“…In contrast, acute ondansetron (0.5 or 50 μg/kg, i.v.) did not affect DRN 5-HT neuronal firing rate (Adrien et al, 1992). In line with previous reports, acute paroxetine administration dose-dependently suppressed 5-HT neuronal firing in the DRN (Hajos et al, 1995).…”

Section: Discussionsupporting

confidence: 74%

A 5-HT3 receptor antagonist potentiates the behavioral, neurochemical and electrophysiological actions of an SSRI antidepressant

Bétry

Overstreet

Haddjeri

et al. 2015

Pharmacology Biochemistry and Behavior

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Section: Discussionsupporting

confidence: 74%

A 5-HT3 receptor antagonist potentiates the behavioral, neurochemical and electrophysiological actions of an SSRI antidepressant

Bétry

Overstreet

Haddjeri

et al. 2015

Pharmacology Biochemistry and Behavior

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“…In a re cent study (Lecrubier et a1. 1993), a statistically sig- Similar to our findings, in a previous study in rats, no major sleep EEG findings by SHT3 receptor antag onists were found (Adrien et al 1992). The only changes were that the higher (25 mg) dose of tropisetron slightly reduced stage 2 during the entire night and increased REM sleep during the first third of the night, whereas the amount of REM sleep of the entire night, on aver age, remained stable.…”

Section: Discussionsupporting

confidence: 77%

Effects of 5HT3 Receptor Antagonism by Tropisetron on the Sleep EEG and on Nocturnal Hormone Secretion

Rothe

Güldner

Hohlfeldt

et al. 1994

Neuropsychopharmacol

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Two dosages (5 mg and 25 mg) of the selective 5HT3 receptor antagonist tropisetron (lCS 205-930) were administered to healthy male controls, and the effects on the sleep EEG and nocturnal secretory activity of growth hormone (GH) and cortisol were evaluated. The lower dosage was administered to four subjects and the higher dosage to eight on 5 consecutive days, preceded and followed by 2 days of placebo treatment. After 25 mg of tropisetron, there was a slight increase in REM sleep in the first part of the sleep period, and stage 2 was decreased during the total night. In addition, plasma cortisol levels increased earlier than under placebo, and plasma GH levels were reduced in the second part of the night. Thus, only discrete effects of tropisetron upon sleep-endocrine activity were noted, making it unlikely that serotoninergic neurotransmission exerts its well documented effects upon sleep through 5HT3 receptors.

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“…While the present results in humans are consistent with preclinical studies indicating that serotonergic agonists, acting at the 5HT1A receptor on cholinergic neurons, inhibit REM sleep, the current methodology does not address the neuroanatomic sites or precise pharmacological mechanisms of action of orally administered ipsapirone on sleep mechanisms. For example, ipsapirone is also known to directly reduce neuronal discharge in the dorsal raphe, possibly by stimulation of somatodendritic 5-HT1A receptors (Adrien et al 1992). Furthermore, with the recent cloning of the 5-HT7 receptor, it has been suggested that some 5HT1A receptor agonists are active on this newly discovered receptor and may influence circadian sleep-wake activity (Lovenberg et al 1993).…”

Section: Resultsmentioning

confidence: 97%

Inhibition of REM sleep by ipsapirone, A 5HT1A agonist, in normal volunteers

et al. 1994

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In order to test the hypothesis that serotonergic mechanisms inhibit REM sleep via a 5HT1A receptor, we administered placebo and ipsapirone (10 and 20 mg by mouth 15 min before bedtime) to ten normal volunteers in a double blind fashion. Ipsapirone is a relatively selective 5HT1A receptor agonist. As predicted, ipsapirone prolonged REM latency and Mean Latency to Eye Movements (M-LEM), a measure of time between onset of REM sleep and the first eye movement of the REM period, and REM% at both doses compared with placebo. It also reduced sleep efficiency and total REM sleep time at the highest dose. These results support the hypothesis that systemic stimulation of 5HT1A receptors prolong REM latency and inhibit REM sleep.

show abstract

Central action of 5-HT3 receptor ligands in the regulation of sleep-wakefulness and raphe neuronal activity in the rat

Cited by 34 publications

References 26 publications

A 5-HT3 receptor antagonist potentiates the behavioral, neurochemical and electrophysiological actions of an SSRI antidepressant

A 5-HT3 receptor antagonist potentiates the behavioral, neurochemical and electrophysiological actions of an SSRI antidepressant

Effects of 5HT3 Receptor Antagonism by Tropisetron on the Sleep EEG and on Nocturnal Hormone Secretion

Inhibition of REM sleep by ipsapirone, A 5HT1A agonist, in normal volunteers

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