Acetylcholine and the Regulation of REM Sleep: Basic Mechanisms and Clinical Implications for Affective Illness and Narcolepsy

Shiromani, Priyattam J.; Gillin, J. Christian; Henriksen, Steven J.

doi:10.1146/annurev.pa.27.040187.001033

Cited by 112 publications

(26 citation statements)

References 30 publications

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“…Basic and clinical studies have demonstrated the involvement of muscarinic cholinergic systems in the regulation of REM sleep (George et al 1974;Hobson et al 1993;Jones 1993;Shiromani and Gillin 1987). While acute administration of muscarinic agonists can shorten REM latency, increase REM activity and REM density, and reduce slow-wave sleep (Berkowitz et al 1990;Riemann and Berger 1989;Riemann et al 1988;Sitaram and Gillin 1980;Sitaram et al 1977Sitaram et al , 1978, acute administration of muscarinic cholinergic antagonists generally produce the opposite effects (Gillin et al 1991b;Hohagen et al 1994;Poland et al 1989Poland et al , 1997Sagalés et al 1969;Salin-Pascual et al 1993;Sitaram et al 1978).…”

Section: Discussionmentioning

confidence: 99%

Age-Related Effects of Scopolamine on REM Sleep Regulation in Normal Control Subjects Relationship to Sleep Abnormalities in Depression

Rao

Lutchmansingh

Poland

1999

Neuropsychopharmacology

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In order to assess the influence of development on the regulation of rapid eye movement (REM) sleep by cholinergic systems, the REM sleep responses toElectroencephalographic (EEG) sleep changes associated with major depressive disorder are among the most well replicated findings in adult patients (for a review, see Benca et al. 1992). Perhaps the most dramatic changes occur with respect to rapid eye movement (REM) sleep measures.Despite the evidence for continuities in mood disorders across the life span (Kovacs 1996), the manifestation of comparable REM sleep abnormalities appears to occur less frequently in early onset depression (reviewed in Rao et al. 1996). The mechanisms for this disparity are unclear. One possibility is that circadian and ultradian rhythms are more desynchronized in youngsters with depression, thus not allowing the REM sleep abnormalities, particularly the shortening of REM latency, to be easily detected (Teicher et al. 1993). Another possibility is that slow-wave sleep pressure is greater than REM sleep pressure in youngsters so that the shortening of REM sleep latency is constrained (Borbely 1982).Furthermore, it is possible that the neurotransmitter circuitry involved in REM sleep regulation is not fully mature in youngsters. Thus, shortened REM latency or increased REM activity and density in depression

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Section: Discussionmentioning

confidence: 99%

Age-Related Effects of Scopolamine on REM Sleep Regulation in Normal Control Subjects Relationship to Sleep Abnormalities in Depression

Rao

Lutchmansingh

Poland

1999

Neuropsychopharmacology

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“…Second, as pointed out by Zoltoski et al (1993), the hypothesis that REM sleep was triggered by M2 mus carinic receptors arose from studies in which relatively selective muscarinic agonists and antagonists were ap plied to the medial pontine reticular formation (Hob son et al 1986;Shiromani et al 1987). Thus, it might be that other anatomical sites, including those with M1 receptors, can modify or modulate the onset, main te nance, or nature of REM sleep (Zoltoski et al 1993).…”

Section: Discussionmentioning

confidence: 99%

“…Both drugs suppressed rapid eye movement (REM) sleep as reflected by an increase of REM latency and a decrease in the KEY WORDS: Bornaprine; Biperiden; Cholinergic system; REM sleep; Slow wave sleep There is strong evidence that the cholinergic system is involved in the generation of rapid eye movement (REM) sleep (Hobson et al 1986). Whereas the trigger ing of REM sleep by cholinergic neurons has been demonstrated convincingly (Hobson et al 1975(Hobson et al , 1986Shiromani et al 1987), it is still a question as to the ex tent muscarinic M1 and/or M2 receptors are involved in REM sleep regulation. Results of a recent study based on the microinjection of cholinomimetic drugs at the medial pontine-reticular formation in cats suggest that physiological and cholinergically induced REM sleep is mediated primarily by the M2 subtype of muscarinic receptors (Velazquez-Moctezuma et al 1989, 1990.…”

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confidence: 99%

Influence of Biperiden and Bornaprine on Sleep in Healthy Subjects

Hohagen

Lis

Riemann

et al. 1994

Neuropsychopharmacol

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mg, an anticholinergic drug that is relatively selective for the Ml receptor subtype, and bornaprine, 4 mg, a nonselective Ml and M2 antagonist, were administered orally in a randomized, double-blind design to twelve healthy volunteers to investigate the effect on polysomnographically recorded sleep. Both drugs suppressed rapid eye movement (REM) sleep as reflected by an increase of REM latency and a decrease in the KEY WORDS: Bornaprine; Biperiden; Cholinergic system; REM sleep; Slow wave sleep There is strong evidence that the cholinergic system is involved in the generation of rapid eye movement (REM) sleep (Hobson et al. 1986). Whereas the trigger ing of REM sleep by cholinergic neurons has been demonstrated convincingly (Hobson et al. 1975(Hobson et al. , 1986Shiromani et al. 1987), it is still a question as to the ex tent muscarinic M1 and/or M2 receptors are involved in REM sleep regulation. Results of a recent study based on the microinjection of cholinomimetic drugs at the medial pontine-reticular formation in cats suggest that physiological and cholinergically induced REM sleep is mediated primarily by the M2 subtype of muscarinic receptors (Velazquez-Moctezuma et al. 1989, 1990. In comparison, biperiden, a preferential M1 antagonist, increased REM sleep latency, and reduced REM sleep time in healthy volunteers (Gillin et al. 1991;Salin Pascual et al. 1991.The aim of the present study was to investigate the effect of biperiden and bomaprine, two cholinergic an tagonists, on sleep, especially REM sleep, in healthy subjects. The pharmacokinetic properties of both drugs are similar (Hollmann et al. 1984;Grimaldi et al. 1986;Mayo et al. 1980). Biperiden is considered to be a highly selective M1 antagonist (Burke 1986; Syvalahti et al. 1988;Eltze and Figala 1988;Freedman et al. , 1988) with a M1 selectivity similar to that of pirenzepine (Syvalahti et al. 1987;Avissar and Schreiber 1989;Larson et al. 1991). Bomaprine, another centrally acting anticholiner gic drug, lacks selectivity for the M1 or M2 receptor hav ing equal affi nity to both receptor subtypes (Kreiskott and Kretschmar 1985). The antagonism of bomaprine at the M2 muscarinic receptor has been demonstrated (Huff ord et al., 1991). If M2 receptors are mainly respon sible for the generation of REM sleep, a nonselective anticholinergic drug like bomaprine, that also shows M2 antagonistic properties, should have stronger REM sleep-suppressing effects compared to a preferential M1 receptor antagonist like biperiden. SUBJECTS AND METHODSWe investigated 12 healthy volunteers with a mean age (±SD) of 25.01 ± 1.9 years (range 22-28 years) who

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“…This suggests that SS and CST both have sleep regulatory functions and probably interplay in the regulation of sleep, both in their own specific way. Previous studies demonstrated that acetylcholine (ACh) is present at low concentration in the cortex during slow-wave sleep, and higher concentrations of ACh are associated with wakefulness and REM sleep (Shiromani et al, 1987). Therefore, the question was addressed whether CST produces its sleep promoting effects by modulating ACh activity.…”

Section: Central Actions In the Ss/cst And Sst Networkmentioning

confidence: 99%

Future clinical prospects in somatostatin/cortistatin/somatostatin receptor field

Dalm¹,

Hofland²,

Lamberts³

2008

Molecular and Cellular Endocrinology

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Acetylcholine and the Regulation of REM Sleep: Basic Mechanisms and Clinical Implications for Affective Illness and Narcolepsy

Cited by 112 publications

References 30 publications

Age-Related Effects of Scopolamine on REM Sleep Regulation in Normal Control Subjects Relationship to Sleep Abnormalities in Depression

Age-Related Effects of Scopolamine on REM Sleep Regulation in Normal Control Subjects Relationship to Sleep Abnormalities in Depression

Influence of Biperiden and Bornaprine on Sleep in Healthy Subjects

Future clinical prospects in somatostatin/cortistatin/somatostatin receptor field

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