Inhibition of REM sleep by fluoxetine, a specific inhibitor of serotonin uptake

Slater, Irwin H.; Jones, G. T.; Moore, R Andrew

doi:10.1016/0028-3908(78)90010-2

Cited by 54 publications

(20 citation statements)

References 12 publications

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“…In common with fluoxetine, acute injection of several other SSRIs including sertraline and citalopram have been shown to decrease REMS in the rat, the hamster or the cat (Gao et al, 1992 ;Hilakivi et al, 1987 ;Monaca et al, 2003 ;Pastel and Fernstrom, 1987 ;Ross et al, 1990 ;Slater et al, 1978). Notwithstanding, systemic drug studies have neither elucidated the site of action of fluoxetine nor characterized the 5-HT receptor subtype(s) involved in the suppressive effect on REMS.…”

Section: Discussionmentioning

confidence: 94%

A study of the brain structures involved in the acute effects of fluoxetine on REM sleep in the rat

Monti¹,

Jantos²

2005

Int. J. Neuropsychopharm.

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The effects of acute administration of fluoxetine, a selective serotonin reuptake inhibitor on spontaneous sleep, were studied in adult rats implanted for chronic sleep recordings. Fluoxetine was administered systemically or infused directly into the dorsal raphe nucleus (DRN), the right laterodorsal tegmental nucleus (LDT) or the medial pontine reticular formation (mPRF). Systemic administration of fluoxetine (3.0-12.0 micromol/kg) significantly reduced rapid-eye-movement sleep (REMS) and the number of REM periods; REMS latency was augmented. Direct infusion of fluoxetine (1.0 nmol) into the DRN induced a significant increment of REMS and of the number of REM periods whereas REMS latency was reduced. Microinjection of fluoxetine into the LDT (1.0 nmol) or the mPRF (0.8 nmol) decreased REMS and the number of REM periods whereas REMS latency was augmented. Pre-treatment with the selective 5-HT1A receptor antagonist WAY 100635 prevented the reduction of REMS induced by the microinjection of fluoxetine into the LDT. Our results indicate that the fluoxetine-induced suppression of REMS is related to the inhibition of brainstem structures involved in the promotion and the induction of REMS. The decrease of REMS would be dependent upon the activation of several 5-HT receptor subtypes, including the 5-HT1A receptor.

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Section: Discussionmentioning

confidence: 94%

A study of the brain structures involved in the acute effects of fluoxetine on REM sleep in the rat

Monti¹,

Jantos²

2005

Int. J. Neuropsychopharm.

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“…Fluoxetine reduces REM sleep (Vogel et al 1975;Fuller etal. 1976;Slater et al 1978) but it enhances memory retention.…”

Section: Discussionmentioning

confidence: 98%

Fluoxetine enhances memory processing in mice

Flood

Cherkin

1987

Psychopharmacology

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Fluoxetine (FLU) increases brain concentrations of serotonin by blocking its uptake, without appreciably affecting the dopamine or norepinephrine systems. The present experiments provide evidence that a subcutaneous injection of FLU enhanced post-memory processing ("consolidation") and retrieval, but not acquisition in young adult mice. FLU (15 mg/kg) enhanced 1-week memory retention when injected 2 min post-training. Similar enhancement was obtained with intracerebroventricular injection (20 micrograms per mouse). FLU enhanced retention when administered prior to training (1-5 mg/kg). FLU (2.5 mg/kg) enhanced recall scores when injected 1 h before the 1-week retention test, indicating an enhancing effect on memory retrieval. Neither the pre-training nor pre-testing effects depended on improved acquisition, since FLU did not improve acquisition of T-maze foot-shock avoidance over the dose range 0.5-35 mg/kg. The sensitive period for post-training enhancement by FLU (15 mg/kg) was less than 90 min, as shown by the temporal gradient typical of memory-enhancing drugs. The amnesia induced by a protein synthesis inhibitor anisomycin, or by an anticholinergic drug scopolamine, was blocked by FLU (15 mg/kg) injected post-training. Finally, FLU (15 mg/kg) injected after one-trial passive avoidance training enhanced 1-week retention, demonstrating effectiveness in this task as well as in the active avoidance task.

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“…Finally, suggestion of a potential antidepressant/anxiolytic activity was obtained from effects of SSR181507 on the sleep pattern (EcoG activity) in rats. Antidepressants such as fluoxetine and imipramine decrease the time spent in PS by increasing the latency time to enter this stage of sleep (Slater et al, 1978;Kleinlogel, 1982). SSR181507, 3 mg/kg i.p., was found to affect the sleep pattern in a way typical of that of antidepressants.…”

Section: Discussionmentioning

confidence: 99%

SSR181507, A Dopamine D2 Receptor Antagonist and 5-HT1A Receptor Agonist. II: Behavioral Profile Predictive of an Atypical Antipsychotic Activity

Depoortère

Boulay

Perrault

et al. 2003

Neuropsychopharmacol

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monohydrochloride) is a novel tropanemethanamine benzodioxane that displays antagonist activity at dopamine D 2 receptors and agonist activity at 5-HT 1A receptors. SSR181507 antagonized apomorphine-induced climbing in mice and stereotypies in rats (ED 50 of 2 and 3.4 mg/kg i.p., respectively) and blocked D-amphetamine-induced hyperlocomotion in rats at lower doses (0.3-1 mg/kg i.p.). At 1-10 mg/kg, it was found to disrupt active avoidance in mice. SSR181507 did not induce catalepsy in rats (MED460 mg/kg i.p.) and antagonized (3-10 mg/kg i.p.) haloperidol-induced catalepsy. SSR181507 was also active in two models sensitive to antidepressant/ anxiolytic drugs: in a guinea-pig pup/mother separation test, it decreased (1-3 mg/kg i.p.) the time spent vocalizing during the separation episode, and in a lithium-induced taste aversion procedure in rats, it partially reversed (3 mg/kg i.p.) the decrease of intake of a saccharin solution. Furthermore, SSR181507 increased (3 mg/kg i.p.) the latency time to paradoxical sleep in rats, an effect commonly observed with antidepressants. Coadministration of the selective 5-HT 1A blocker SL88.0338 produced catalepsy and antagonized the effects of SSR181507 in the depression/anxiety tests, confirming the view that activation of 5-HT 1A receptors confers an atypical profile on SSR181507, and is responsible for its antidepressant/anxiolytic properties. Finally, SSR181507 (1-3 mg/kg) did not affect memory performance in a Morris water maze task in rats. The pharmacological profile of SSR181507 suggests that it should control the symptoms of schizophrenia, in the absence of extrapyramidal signs and cognitive deficits, with the additional benefit of antidepressant/anxiolytic activities.

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Inhibition of REM sleep by fluoxetine, a specific inhibitor of serotonin uptake

Cited by 54 publications

References 12 publications

A study of the brain structures involved in the acute effects of fluoxetine on REM sleep in the rat

A study of the brain structures involved in the acute effects of fluoxetine on REM sleep in the rat

Fluoxetine enhances memory processing in mice

SSR181507, A Dopamine D2 Receptor Antagonist and 5-HT1A Receptor Agonist. II: Behavioral Profile Predictive of an Atypical Antipsychotic Activity

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