Elsevier

Brain Research

Volume 543, Issue 1, 8 March 1991, Pages 175-179
Brain Research

Cholinergic antagonists and REM sleep generation

https://doi.org/10.1016/0006-8993(91)91064-8Get rights and content

Abstract

In this study we extended our observations on the role of M1 and M2 muscarinic receptors in mediating the cholinergic induction of REM sleep. Cats were chronically implanted with sleep recording electrodes and microinjections of Ringer's or muscarinic antagonists followed by the relatively specific M2 muscarinic agonist, cis-methyl-dioxolane (cisdioxo), were made into the medial pontine reticular formation (mPRF). The microinjection of Ringer's followed by cisdioxo significantly increased REM sleep percentage. Atropine, a mixed muscarinic receptor antagonist, administered before cisdioxo blocked the REM sleep increase while pirenzepine, a selective M1 muscarinic antagonist, did not block the cisdioxo-induced increase in REM sleep. Gallamine, a nicotinic and a putative M2 antagonist, tended to inhibit the cisdioxo-induced increase in REM sleep. These results support the hypothesis that the cholinergic stimulation-induced REM sleep in the medial pontine reticular formation is mediated by a non-M1 muscarinic receptor subtype.

Reference (25)

Cited by (58)

  • The cognitive neuroscience of lucid dreaming

    2019, Neuroscience and Biobehavioral Reviews
    Citation Excerpt :

    As discussed above, lucid dreaming is associated with increased cortical activation (LaBerge et al., 1981a), which reaches its peak during phasic REM sleep. Given the relationship between phasic REM sleep and lucid dreaming, as well as the role of Acetylcholine (ACh) in REM sleep regulation (e.g., Amatruda et al., 1975; Velazquez-Moctezuma et al., 1991), agents acting on the cholinergic system have received particular interest. In an initial pilot study, LaBerge (2001) evaluated the effect of donepezil (Aricept), an Acetylcholinesterase inhibitor (AChEI), on lucid dreaming in a small group of participants (N = 10) who reported prior experience with lucid dreaming.

  • Consciousness and Meta-Consciousness During Sleep <sup>☆</sup>

    2019, Handbook of Behavioral Neuroscience
    Citation Excerpt :

    Research has also explored whether it is possible to induce lucid dreams through pharmacology. Given that lucid dreams tend to occur during periods of increased physiological activation during REM sleep, together with clear evidence that REM sleep is modulated by acetylcholine (ACh) (Baghdoyan, 1997; Gillin et al., 1985; Velazquez-Moctezuma, Shalauta, Gillin, & Shiromani, 1991), agents acting on the cholinergic system have received particular interest. In an initial pilot study, LaBerge (2001) evaluated the impact of either 0 (placebo), 5, or 10 mg of donepezil (Aricept), an acetylcholinesterase inhibitor (AChEI), administered before sleep in a counterbalanced order on three nights in a small group of highly experienced lucid dreamers.

  • Role of histamine H1-receptor on behavioral states and wake maintenance during deficiency of a brain activating system: A study using a knockout mouse model

    2016, Neuropharmacology
    Citation Excerpt :

    Together, both data sets with scopolamine and physostigmine indicate that H1−/− mice responded to cholinergic ligands in a more pronounced manner than their WT littermates. Because of the greater effects seen with the cholinergic ligands in H1−/− mice and in order to assess whether this genotype-related difference was linked to gene expression, we quantified muscarinic receptor (M1–M5) genes because of the importance of this receptor category in cortical activation and sleep-wake control (Imeri et al., 1991, 1996; Vanni-Mercier et al., 1991; Velazquez-Moctezuma et al., 1991; Sakai and Onoe, 1997; Brown et al., 2012). The frontal cortex was chosen for this assay because the cerebral cortex is the ultimate target for cortical activation and because the frontal cortex is known for its predominant role in cognitive functions during W.

  • Neuroimaging in sleep medicine

    2007, Sleep Medicine
    Citation Excerpt :

    Activation of the pontine tegmentum, thalamic nuclei and basal forebrain is in agreement with REM sleep generation mechanisms in animals [31–33]. REM sleep is generated by cholinergic processes arising from brainstem structures, located in the PPT and laterodorsal tegmentum (LDT) [31,34–40], that mediate widespread cortical activation by way of a dorsal pathway innervating the thalamus, and a ventral pathway innervating the basal forebrain [41–44]. Activation of limbic and paralimbic structures, including amygdaloid complexes, hippocampal formation and anterior cingulate cortex, is also a highly reproducible finding [2,3,29].

View all citing articles on Scopus

The authors would like to thank Dr. Leonid Margolin and Mr. Frank Taylor of the VAMC animal research facility for their skillful assistance in surgery and care of the animals.

2

Supported by NIH, VAMC Research Service, and NIMH-38738.

1

Supported by NIH NS25212, American Narcolepsy Association

View full text