The Cholinergic Rapid Eye Movement Induction Test With Arecoline in Depression

Gillin, J. Christian; Sutton, Laura; Ruiz, Caroline; Kelsoe, John R.; Dupont, Renee M.; Darko, Denis F.; Risch, S. Craig; Golshan, Shahrokh; Janowsky, David S.

doi:10.1001/archpsyc.1991.01810270076011

Cited by 96 publications

(34 citation statements)

References 47 publications

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“…These sleepwakefulness alterations in H mice are consistent with the data obtained in various depression models in the rat (Adrien et al, 1991;Dugovic et al, 2000;Nestler et al, 2002;Shiromani et al, 1988). Furthermore, they are reminiscent of sleep impairments observed in depressed patients, notably the sleep fragmentation, the shift towards lighter sleep stages, and the enhanced REM sleep pressure (Benca, 2000;Gillin et al, 1991).…”

Section: Locomotor Activity and Sleep-wakefulness Cycles Under Baselisupporting

confidence: 86%

“…Interestingly, this arecoline-induced facilitation of REM sleep was more marked in H than in NH mice, as observed in depressed patients compared with control subjects (Sitaram and Gillin, 1980). This enhanced facilitation could reflect a cholinergic hypersensitivity at the level of pontine REM sleep control system (Gillin et al, 1991;Seifritz et al, 1998). Along this line, the larger amounts of Sleep regulation in helpless mice D Popa et al REM sleep in H mice under baseline conditions might be explained, at least in part, by a high muscarinic tone (Coleman et al, 2004), just as in the case of FSL (Flinders Sensitive Line) rats, another validated model of depression (Overstreet, 1993).…”

Section: Muscarinic-and 5-ht 1a -Receptor-mediated Regulations Of Remmentioning

confidence: 99%

“…As suggested for these patients, they could be accounted for by an imbalance between cholinergic and serotonergic tones. Such imbalance would be essentially due to an increase in cholinergic tone which would result notably in enhanced REM sleep (Gillin et al, 1991) and more frequent awakenings (Lustberg and Reynolds, 2000).…”

Section: Muscarinic-and 5-ht 1a -Receptor-mediated Regulations Of Remmentioning

confidence: 99%

“…Depression is schematically associated with a general increase in cholinergic and decrease in serotonergic neurotransmission (Gillin et al, 1991;Hasler et al, 2004;Kapitany et al, 1999;Seifritz et al, 1998). To test for the presence of such imbalance between cholinergic and serotonergic function in H mice, we investigated the sleep modifications induced by treatments with agonists of muscarinic and serotonergic 5-HT 1A receptors in both H and NH mice.…”

Section: Introductionmentioning

confidence: 99%

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Homeostatic Regulation of Sleep in a Genetic Model of Depression in the Mouse: Effects of Muscarinic and 5-HT1A Receptor Activation

Popa

Yacoubi²,

Vaugeois³

et al. 2005

Neuropsychopharmacol

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In depressed patients, sleep undergoes marked alterations, especially sleep onset insomnia, sleep fragmentation, and disturbances of the Rapid Eye Movement (REM) sleep. Abnormalities of rest-activity rhythms and of hypothalamic-pituitary-adrenocortical function have also been described in these patients. In the present study, we examined the presence of such abnormalities in a recently developed line of mice (Helpless mice-H) that exhibit depression-like behaviors in validated tests, compared to the nonhelpless (NH) line derived from the same colony. Experiments were essentially carried out in females for which previous studies showed marked differences between H and NH lines. Compared to NH mice, the H line exhibited (i) lower basal locomotor activity, (ii) sleep fragmentation, shift towards lighter sleep stages, and facilitation of REM sleep reflected by increased amounts and decreased latency, (iii) larger response to the REM sleep promoting effect of muscarinic receptor stimulation (by arecoline). In contrast, H and NH mice were equally responsive to the REM sleep inhibitory effect of 5-HT 1A receptor stimulation (by 8-OH-DPAT). In addition, a deficiency in delta power enhancement after sleep deprivation was observed in the H group, and acute immobilization stress in this group failed to elicit a REM sleep rebound and was associated with a long-lasting raise in serum corticosterone levels. These results further validate H mice as a depression model and suggest they might be of particular interest for investigating the neurobiological mechanisms and possibly genetic substrates underlying sleep alterations associated with depression.

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Section: Locomotor Activity and Sleep-wakefulness Cycles Under Baselisupporting

confidence: 86%

Section: Muscarinic-and 5-ht 1a -Receptor-mediated Regulations Of Remmentioning

confidence: 99%

Section: Muscarinic-and 5-ht 1a -Receptor-mediated Regulations Of Remmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Homeostatic Regulation of Sleep in a Genetic Model of Depression in the Mouse: Effects of Muscarinic and 5-HT1A Receptor Activation

Popa

Yacoubi²,

Vaugeois³

et al. 2005

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…The basic mechanisms unraveled in animals are at least partially paralleled in human studies combining EEG sleep with pharmacological probes. For instance, REM sleep is suppressed following systemic 5-HT 1A agonists (Gillin et al 1994;Seifritz et al 1996) and promoted following cholinergic agonists (Sitaram et al 1976;Berger et al 1985;Gillin et al 1991b;. Muscarinic receptor antagonists, on the other hand, partially suppress REM sleep (Gillin et al 1991a), and the depletion of central serotonin enhances REM sleep Moore et al 1998Moore et al , 2001Voderholzer et al 1998).…”

Section: Aspects Of Sleep Regulationmentioning

confidence: 99%