Induction of both emotional behavior and a novel form of REm sleep by chemical stimulation applied to cat mesencephalon

Baxter, Bruce L.

doi:10.1016/0014-4886(69)90059-4

Cited by 140 publications

(17 citation statements)

References 17 publications

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“…These studies have shown that the application of Ach or cholinergic agonist, carbachol, into the brainstem induces REM sleep-like state in the cat. A number of studies from various laboratories confirmed, as well as expanded, those original cholinergic stimulation studies by inducing a REM sleep-like state in the cat via local microinjection of pharmacological agents that increase Ach by blocking its natural degradation or via activation cholinergic receptors in the mPRF (Amatruda et al, 1975;Baghdoyan et al, 1984aBaghdoyan et al, , b, 1987Baxter, 1969;Hobson et al, 1983;Kostowski, 1971;Quattrochi et al, 1989;Shiromani and McGinty, 1986;Vanni-Mercier et al, 1989;Velazquez-Moctezuma et al, 1989Yamamoto et al, 1990a;Yamuy et al, 1993). Microinjection of similar agents in rats also yields a comparative induction of a REM sleep-like state (Bourgin et al, 1995;Gnadt and Pegram, 1986;Kubin, 2001;Marks and Birabil, 1998;Shiromani and Fishbein, 1986).…”

Section: Relationship Between the Ppt Cholinergic Cells And Glutamatementioning

confidence: 88%

Neurobiological mechanisms for the regulation of mammalian sleep–wake behavior: Reinterpretation of historical evidence and inclusion of contemporary cellular and molecular evidence

Datta

MacLean

2007

Neuroscience & Biobehavioral Reviews

268

249

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At its most basic level, the function of mammalian sleep can be described as a restorative process of the brain and body; recently, however, progressive research has revealed a host of vital functions to which sleep is essential. Although many excellent reviews on sleep behavior have been published, none have incorporated contemporary studies examining the molecular mechanisms that govern the various stages of sleep. Utilizing a holistic approach, this review is focused on the basic mechanisms involved in the transition from wakefulness, initiation of sleep and the subsequent generation of slow-wave sleep and rapid eye movement (REM) sleep. Additionally, using recent molecular studies and experimental evidence that provides a direct link to sleep as a behavior, we have developed a new model, the cellular-molecular-network model, explaining the mechanisms responsible for regulating REM sleep. By analyzing the fundamental neurobiological mechanisms responsible for the generation and maintenance of sleep-wake behavior in mammals, we intend to provide a broader understanding of our present knowledge in the field of sleep research.

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Section: Relationship Between the Ppt Cholinergic Cells And Glutamatementioning

confidence: 88%

Neurobiological mechanisms for the regulation of mammalian sleep–wake behavior: Reinterpretation of historical evidence and inclusion of contemporary cellular and molecular evidence

Datta

MacLean

2007

Neuroscience & Biobehavioral Reviews

268

249

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“…Both systems are critically involved in behavioral states, with the ascending cholinergic system for the cortical activation during wakefulness and paradoxical sleep (PS) and the pontomedullary system for the sensory and motor inhibition that occurs during PS (Sakai, 1985;Jones, 1985Jones, , 1990. Pharmacological studies have long indicated that the stimulation of pontine cholinergic structures readily induces the polygraphic signs of PS in the cat, the rat, and the dog (Amatruda et al, 1975;Baghdoyan et al, 1984;Baxter, 1969;Brodie and Proudfit, 1984;George et al, 1964;Katayama et al, 1984;Mitler and Dement, 1974;Valazquez-Mozezuma et al, 1989;Quattrochi et al, 1989;Reid et al, 1994a).…”

Section: Indexing Terms: Narcolepsy; Acetylcholine; Norepinephrine; Pmentioning

confidence: 97%

Mesopontine organization of cholinergic and catecholaminergic cell groups in the normal and narcoleptic dog

et al. 1997

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Canine narcolepsy is a unique experimental model of a human sleep disorder characterized by excessive daytime sleepiness and cataplexy. There is a consensus recognition of an imbalance between cholinergic and catecholaminergic systems in narcolepsy although the underlying mechanisms remain poorly understood. Possible substrates could be an abnormal organization, numbers and/or ratio of cholinergic to catecholaminergic cells in the brain of narcoleptic dogs. Therefore, we sought to characterize the corresponding neuronal populations in normal and narcoleptic dogs (Doberman Pinscher) by using choline acetyltransferase (ChAT), nicotinamide adenosine dinucleotide phosphate (NADPH)-diaphorase, tyrosine hydroxylase (TH), and dopamine beta-hydroxylase (DBH). Cholinergic cell groups were found in an area extending from the central to the gigantocellular tegmental field and the periventricular gray corresponding to the pedunculopontine tegmental nucleus (PPT), the laterodorsal tegmental nucleus (LDT), and the parabrachial nucleus. An almost perfect co-localization of ChAT and NADPH-diaphorase was also observed. Catecholaminergic cell groups detected included the ventral tegmental area, the substantia nigra, and the locus coeruleus nucleus (LC). The anatomical distribution of catecholaminergic neurons was unusual in the dog in two important aspects: i) TH- and/or DBH-immunoreactive neurons of the LC were found almost exclusively in the reticular formation and not within the periventricular gray, ii) very few, if any TH-positive neurons were found in the central gray and dorsal raphe. Quantitative analysis did not reveal any significant differences in the organization and the number of cells identified in the LDT, PPT, and LC of normal and narcoleptic dogs. Moreover, the cholinergic to catecholaminergic ratio was found identical in the two groups. In conclusion, the present results do not support the hypothesis that the neurochemical imbalance in narcolepsy could result from abnormal organization, numbers, or ratio of the corresponding neuronal populations.

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“…The lust response was indistinguishable physiologically from REM sleep (EEG activation, REM's, hippocampal theta, EMG suppression, miotic pupils) except that it was of greater duration; in the second response, the cats showed EEG activation and EMG suppression; in neither type of response could EMG suppression be blocked by auditory, tactile, or reticular stimulation. Baxter (1969) reported that crystalline carbachol produced prolonged episodes of REM-like sleep about 9-14 min after placement in the mesencephalic central grey, possibly with diffusion into the ventricular system. As in the REM-like state observed by George et al, (1964), that produced by Baxter was characterized by complete lack of arousal to strong external stimulation; Baxter reported, for example, unresponsiveness to surgical incision.…”

Section: Previous Pharmacological Studies Of Ach and Sleepmentioning

confidence: 98%

Acetylcholine: Possible Involvement in Sleep and Analgesia

Sitaram

Gillin

1979

Brain Acetylcholine and Neuropsychiatric Disease

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Induction of both emotional behavior and a novel form of REm sleep by chemical stimulation applied to cat mesencephalon

Cited by 140 publications

References 17 publications

Neurobiological mechanisms for the regulation of mammalian sleep–wake behavior: Reinterpretation of historical evidence and inclusion of contemporary cellular and molecular evidence

Neurobiological mechanisms for the regulation of mammalian sleep–wake behavior: Reinterpretation of historical evidence and inclusion of contemporary cellular and molecular evidence

Mesopontine organization of cholinergic and catecholaminergic cell groups in the normal and narcoleptic dog

Acetylcholine: Possible Involvement in Sleep and Analgesia

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