Comparison of the effects of two ‘sleep’ peptides, delta sleep-inducing peptide and arginine-vasotocin, on single neurons in the rat and rabbit brain stem

Normanton, J.R.; Gent, J P

doi:10.1016/0306-4522(83)90029-5

Cited by 51 publications

(5 citation statements)

References 17 publications

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“…It therefore appears that substances possessing neuroexcirant (DSIP, [85]) and/or emetogenic (neurotensin, angiotensin II, met-enkephalin; [86]) activity do not necessarily exert deglutitive stimulant actions. On the other hand, the cardiac glycoside ouabain is an effective deglutitive stimulant in this experimental model, although it preferentially activates the buccopharyngeal stage.…”

Section: Miscellaneous Agents: Emetogenic Vs "'Pro-deglutitive'" Agentsmentioning

confidence: 97%

Neuropharmacologic correlates of deglutition: Lessons from fictive swallowing

Bieger

1991

Dysphagia

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Pharmacologic investigations into the transmission processes underlying fictive swallowing in the rat have disclosed the potential diversity of chemical signals used in central deglutitive pathways. Monoaminergic mechanisms appear to serve as links between subcortical structures and the medullary pattern generator of swallowing (PGS), and may play a critical role in maintaining internal facilitatory drive, required by the PGS for optimal responsivity to peripheral sensory input. Cholinergic bulbar interneurons form an integral component of the PGS subnetwork controlling esophageal peristalsis. Local GABA neurons exert a tonic inhibition of the buccopharyngeal stage, may regulate buccopharyngeal-esophageal coupling, and may contribute to peristaltic rhythmic generation at both the premotoneuronal and motoneuronal level. Receptor subtypes for excitatory amino acids (glutamate, aspartate) are differentially associated with deglutitive premotoneurons for both the buccopharyngeal and esophageal stage, as well as with ambiguus motoneurons. Preliminary evidence suggests the existence of excitatory peptidergic mechanisms involving thyrotropin-releasing hormone, vasopressin, oxytocin, and somatostatin, a probable candidate for excitatory transmitter in the solitarioambigual internuncial projection to motoneurons innervating esophageal striated musculature. Further validation of this experimental model may ultimately help to establish a framework for the clinical recognition, management, and exploitation of drug actions on central deglutitive neuroeffectors.

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Section: Miscellaneous Agents: Emetogenic Vs "'Pro-deglutitive'" Agentsmentioning

confidence: 97%

Neuropharmacologic correlates of deglutition: Lessons from fictive swallowing

Bieger

1991

Dysphagia

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“…Pinealectomy (Mouret, Coindet & Couvet 1974) and injection of specific AVT antisera have been shown to induce a narcolepticlike distribution of REM sleep, with profound but reversible effects on both NREM and REM sleep being noted following LHB lesions (Goldstein 1983a). Early work carried out in my own laboratory showed that AVT, applied by microiontophoresis, could induce profound, longlasting (up to 10 min) excitations of central neurones followed by long-duration (50-90 min) desensitization (Normanton & Gent 1983); more recently such observations have also been noted in the LHB (Normanton & Lovick, unpublished data). A DRNpineal inhibitory pathway has been demonstrated (L6ger, Degueurce, Lundberg, Pujol & M0llgard 1983), leading to the suggestion that the pineal gland may be controlled, at least in part, by a tonic inhibitory input from the DRN.…”

Section: Discussionmentioning

confidence: 93%

Reciprocal interactions in the brain stem, REM sleep, and the generation of generalized convulsions

Elazar¹

1986

Behav Brain Sci

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As neurophysiological investigations of sleep cycle control have provided an increasingly detailed picture of events at the cellular level, the concept that the sleep cycle is generated by the interaction of multiple, anatomically distributed sets of neurons has gradually replaced the hypothesis that sleep is generated by a single, highly localized neuronal oscillator.Cell groups that discharge during rapid-eye-movement (REM) sleep (REM-on) and neurons that slow or cease firing during REM sleep (REM-off) have long been thought to comprise at least two neurochemically distinct populations. The fact that putatively cholinoceptive and/or cholinergic (REM-on) and putatively aminergic (REM-off) cell populations discharge reciprocally over the sleep cycle suggests a causal interdependence.In some brain stem areas these cell groups are not anatomically segregated and may instead be neurochemically mixed (interpenetrated). This finding raises important theoretical and practical issues not anticipated in the original reciprocal-interaction model. The electrophysiological evidence concerning the REM-on and REM-off cell groups suggests a gradient of sleep-dependent membrane excitability changes that may be a function of the connectivity strength within an anatomically distributed neuronal network. The connectivity strength may be influenced by the degree of neurochemical interpenetration between the REM-on and REM-offcells. Recognition of these complexities forces us to revise the reciprocal-interaction model and to seek new methods to test its tenets.Cholinergic microinjection experiments indicate that some populations of REM-on cells can execute specific portions of the REM sleep syndrome or block the generation of REM sleep. This observation suggests that the order of activation within the anatomically distributed generator populations may be critical in determining behavioral outcome. Support for the cholinergic tenets of the reciprocal-interaction model has been reinforced by observations from sleep-disorders medicine.Specific predictions of the reciprocal-interaction model and suggestions for testing these predictions are enumerated for future experimental programs that aim to understand the cellular and molecular basis of the mammalian sleep cycle.

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“…Alternatively, intermediate-term treat ment possibly accumulates the actions of DSIP on brain functions and thus induces fundamental changes of physiological mech anisms. The theory that the neuropeptide DSIP is an endogenous neuromodulator of sleep has recently obtained further support by finding DSIP-containing cells and path ways in the limbic system and hypothalamus [24], binding sites for DSIP in the nucleus reticularis giganto-cellularis of the brain stem, a structure involved in the regulation of the sleep-wakefulness rhythm [25], and excitatory actions of DSIP at the single-neu ron level of this structure [26]. On this back ground it seems likely that DSIP administra tion reinforces normal physiological func tions.…”

Section: Discussionmentioning

confidence: 99%

Effects of Delta-Sleep-Inducing Peptide on 24-Hour Sleep-Wake Behaviour in Severe Chronic Insomnia

Schneider-Helmert¹

1987

Eur Neurol

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Impaired daytime functions are a significant part of chronic insomnia besides sleep disturbance. Therefore, the effects of intermediate-term delta-sleep-inducing peptide (DSIP) administration on sleep and daytime performance were investigated in 14 middle-aged chronic insomniacs. DSIP was administered under placebo-controlled, double-blind conditions for 7 successive nights. Polysomnograms were obtained for placebo baseline, beginning and end of DSIP treatment, and one placebo posttreatment night; daytime psychological state and mental performance were extensively tested before and after 6 DSIP injections. The treatment substantially improved night sleep with the first and additionally with repeated doses. These effects were maintained for the first posttreatment (placebo) night. Efficiency of night sleep and daytime rest reached the levels of normal controls. Alertness and performance at daytime increased significantly. The study demonstrates the efficacy of DSIP for the treatment of impaired sleep and daytime functions as well.

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Comparison of the effects of two ‘sleep’ peptides, delta sleep-inducing peptide and arginine-vasotocin, on single neurons in the rat and rabbit brain stem

Cited by 51 publications

References 17 publications

Neuropharmacologic correlates of deglutition: Lessons from fictive swallowing

Neuropharmacologic correlates of deglutition: Lessons from fictive swallowing

Reciprocal interactions in the brain stem, REM sleep, and the generation of generalized convulsions

Effects of Delta-Sleep-Inducing Peptide on 24-Hour Sleep-Wake Behaviour in Severe Chronic Insomnia

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