A cholinergic mechanism in the brainstem reticular formation: Induction of paradoxical sleep

George, Rani Mary; Haslett, Wilford L.; Jenden, Donald J.

doi:10.1016/0028-3908(64)90076-0

Cited by 369 publications

(113 citation statements)

References 13 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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“…Application of acetylcholine (ACh) (George et al, 1964;Lai and Siegel, 1988;Kodama et al, 1990;Reinoso-Suarez et al, 1994), glutamate (Lai and Siegel, 1991;Onoe and Sakai, 1995), corticotropin-releasing factor (Lai and Siegel, 1992), and GABA antagonist (Xi et al, 2001) to the PIA can trigger muscle atonia and REM sleep.…”

Section: Introductionmentioning

confidence: 99%

Changes in Inhibitory Amino Acid Release Linked to Pontine-Induced Atonia: AnIn VivoMicrodialysis Study

2003

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We hypothesized that cessation of brainstem monoaminergic systems and an activation of brainstem inhibitory systems are both involved in pontine inhibitory area (PIA) stimulation-induced muscle atonia. In our previous study (Lai et al., 2001), we found a decrease in norepinephrine and serotonin release in motoneuron pools during PIA stimulation-induced muscle tone suppression. We now demonstrate an increase in inhibitory amino acid release in motor nuclei during PIA stimulation in the decerebrate cat using in vivo microdialysis and HPLC analysis techniques. Microinjection of acetylcholine into the PIA elicited muscle atonia and simultaneously produced a significant increase in both glycine and GABA release in both the hypoglossal nucleus and the lumbar ventral horn. Glycine release increased by 74% in the hypoglossal nucleus and 50% in the spinal cord. GABA release increased by 31% in the hypoglossal nucleus and 64% in the spinal cord during atonia induced by cholinergic stimulation of the PIA. As with cholinergic stimulation, 300 msec train electrical stimulation of the PIA elicited a significant increase in glycine release in the hypoglossal nucleus and ventral horn. GABA release was significantly increased in the hypoglossal nucleus but not in the spinal cord during electrical stimulation of the PIA. Glutamate release in the motor nuclei was not significantly altered during atonia induced by electrical or acetylcholine stimulation of the PIA. We suggest that both glycine and GABA play important roles in the regulation of upper airway and postural muscle tone. A combination of decreased monoamine and increased inhibitory amino acid release in motoneuron pools causes PIA-induced atonia and may be involved in atonia linked to rapid eye-movement sleep.

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“…Reports demonstrating that paradoxical sleep may be induced by intraventricular injection of oxotremorine or carbachol and blocked by atropine sulphate suggest that acetylcholine may be involved in paradoxical sleep (George, Haslett & Jenden, 1964;Khazan & Sawyer, 1964;Khazan, Bar & Sulman, 1967). Moreover, the rate of acetylcholine liberation from the cortical surface of cats is greater during paradoxical sleep than in slow wave sleep (Jasper & Tessier, 1971).…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E₁ causes sedation and increases 5‐hydroxytryptamine turnover in rat brain

Haubrich

Pérez-Cruet

Reid

1973

British J Pharmacology

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Summary1. Administration of prostaglandin E1 (1 mg/kg, i.p.) to rats induced sedation and a decrease in muscular tone. Prostaglandin El-induced sedation was accompanied by the low voltage-high frequency E.E.G. pattern characteristic of the waking animal. 2. Administration of prostaglandin E1 also increased the turnover rate of 5-hydroxytryptamine and raised the concentration of acetylcholine in brain. 3. The behavioural effects of prostaglandin were blocked by prior administration of p-chlorophenylalanine or pargyline, drugs which lowered the brain concentration of 5-hydroxyindoleacetic acid (5-HIAA), and was potentiated by pretreatment with probenecid, which elevated the 5-HIAA concentration. Pretreatment with atropine sulphate failed to alter prostaglandin El-induced sedation. 4. The results are compatible with the possibility that prostaglandin E1 induces a state resembling paradoxical sleep through an action on 5-hydroxytryptamine metabolism in brain.

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A cholinergic mechanism in the brainstem reticular formation: Induction of paradoxical sleep

Cited by 369 publications

References 13 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

Changes in Inhibitory Amino Acid Release Linked to Pontine-Induced Atonia: AnIn VivoMicrodialysis Study

Prostaglandin E₁ causes sedation and increases 5‐hydroxytryptamine turnover in rat brain

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A cholinergic mechanism in the brainstem reticular formation: Induction of paradoxical sleep

Cited by 369 publications

References 13 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

Changes in Inhibitory Amino Acid Release Linked to Pontine-Induced Atonia: AnIn VivoMicrodialysis Study

Prostaglandin E1 causes sedation and increases 5‐hydroxytryptamine turnover in rat brain

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Prostaglandin E₁ causes sedation and increases 5‐hydroxytryptamine turnover in rat brain