Alterations in the sleep-waking cycle induced by cooling of the locus coeruleus area

Cespuglio, Raymond; Gomez, M.E; Faradji, H.; Jouvet, Michel

doi:10.1016/0013-4694(82)90042-6

Cited by 104 publications

(18 citation statements)

References 32 publications

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“…The increased REMS was due to an increase in both the REMS duration per episode as well as the REMS frequency of occurrence. The results of this study may be supported by those of previous studies in which the inactivation of LC neurons either by local cooling (Cespuglio et al, 1982) or by chemical withdrawal of inhibition (Mallick et al, 2001; Chen et al, 2010) increased REMS, while the activation of LC neurons reduced REMS (Singh and Mallick, 1996; Kaur et al, 2001; Carter et al, 2010; Jaiswal et al, 2010). …”

Section: Discussionsupporting

confidence: 88%

Noradrenaline from Locus Coeruleus Neurons Acts on Pedunculo-Pontine Neurons to Prevent REM Sleep and Induces Its Loss-Associated Effects in Rats

Khanday

Somarajan

Mehta

et al. 2016

eNeuro

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Section: Discussionsupporting

confidence: 88%

Noradrenaline from Locus Coeruleus Neurons Acts on Pedunculo-Pontine Neurons to Prevent REM Sleep and Induces Its Loss-Associated Effects in Rats

Khanday

Somarajan

Mehta

et al. 2016

eNeuro

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“…These single cell activity patterns suggest that the reduction of NE release due to withdrawal of noradrenergic cell activity could be an important step for the induction of REM sleep. The significance of this cessation of noradrenergic cell activity, immediately before and during REM sleep, was expanded by the demonstration that unilateral and bilateral cooling of the LC in the behaving cats induced a transitional stage between SWS and REM sleep within 3 min and within 4 min total REM sleep was achieved (Cespuglio et al, 1982). This study was significant because the localized cooling suppresses neuronal activity in the LC and reduction of noradrenergic cell activity induced REM sleep.…”

Section: Noradrenergic Cells In the Lcmentioning

confidence: 95%

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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“…Previous experiments have in fact documented that during sleep-awake stages there is a change in the bioelectric activity of single units in the locus coeruleus (Steriade & Hobson, 1976;Clark, 1979;Ramm, 1979;Aston-Jones & Bloom, 1981ab;Cespuglio et al, 1982). Furthermore, in previous experiments we have shown that the direct microinfusion of agonists at a2-adrenoceptors into the LC produces dose-dependent behavioural sleep and ECoG synchronization (De Sarro et al, 1987;1988a).…”

Section: Discussionmentioning

confidence: 95%

Different profile of electrocortical power spectrum changes after micro‐infusion into the locus coeruleus of selective agonists at various opioid receptor subtypes in rats

Bagetta

Sarro

Sakurada

et al. 1990

British J Pharmacology

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1 The effects of various opioid receptor agonists given directly by means of a chronically implanted cannula into the locus coeruleus (LC) on behaviour and ECoG activity, continuously analysed, and quantified as total power spectrum (0)(1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16) and in preselected frequency [3][4][5][6][6][7][8][9][9][10][11][12], were studied in rats. 2 Dermorphin (0.05, 0.5, 1, 2 and 5 pmol) and Tyr-D-Ala-Gly-N-Me-Phe-Gly-ol (DAMGO; 1, 10, 30, 100 pmol and 1 nmol), two typical p-receptor agonists, applied unilaterally or bilaterally directly into the LC, produced a typical dose-dependent ECoG synchronization with a significant increase in total power spectrum as well as in the lower frequency bands. Dermorphin was found to be approximately 30 times more powerful than DAMGO in producing similar quantitative ECoG changes. 3 D-Ala-D-Leu-Thr-Gly-Gly-Phe-Leu (DADLE; 1, 10, 50 and 1OOpmol), a selective 5-receptor agonist, micro-infused into the LC produced dose-dependent behavioural soporific effects and ECoG increase in total power spectrum as well as in 3-6, 6-9, 9-12 Hz frequency bands. In comparison to dermorphin, the ECoG power spectrum effects of DADLE were 10 fold less potent, whereas in comparison to DAMGO it was approximately 3 times more potent. A lower dose (0.1 pmol) was ineffective in changing behaviour and ECoG power spectrum. 4 The microinfusion into the LC of U 50, 488H, a selective K-opioid receptor agonist, (0.25, 1, 2.5, 5 and lOpmol) produced a typical pattern characterized by a first short-lasting (3-25 min) phase of behavioural arousal and ECoG desynchronization, followed by a longer lasting (20-130min according to the dose) phase of behavioural sleep and ECoG synchronization. A lower dose (0.1 pmol) was ineffective in changing behaviour and ECoG power spectrum. 5Dextromethorphan and ketamine, two selective agonists at a-receptors given into the LC (1, 5 and 1Opmol) induce behavioural arousal, increase in locomotor activity and an intense pattern of stereotyped movements. However, by increasing the dose of ketamine (50 and lOOpmol), marked sedation, postural changes and an increase in low frequency ECoG bands, sometimes associated with high amplitude fast frequency potentials, were observed. 6 Naloxone applied directly into the LC (1 and 2 pmol 15min before) was able to prevent the behavioural and ECoG effects induced by dermorphin, DAMGO and DADLE. Higher doses of naloxone (1Opmol into the LC) were however, required to antagonize the behavioural and ECoG soporific effects induced by the K-receptor agonist U 50,488H. In contrast, naloxone (1Opmol into the LC) was unable to prevent or reduce the behavioural and ECoG effects induced by subsequent administration into the same site of dextromethorphan and ketamine. 7 In conclusion, the present experiments confirm that behavioural and ECoG effects elicited following stimulation of a-, b-, K-and e-opioid receptors located in the LC are quite different. Activation of ,u-, band K-receptors induced sedative effects whereas d...

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Alterations in the sleep-waking cycle induced by cooling of the locus coeruleus area

Cited by 104 publications

References 32 publications

Noradrenaline from Locus Coeruleus Neurons Acts on Pedunculo-Pontine Neurons to Prevent REM Sleep and Induces Its Loss-Associated Effects in Rats

Noradrenaline from Locus Coeruleus Neurons Acts on Pedunculo-Pontine Neurons to Prevent REM Sleep and Induces Its Loss-Associated Effects in Rats

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

Different profile of electrocortical power spectrum changes after micro‐infusion into the locus coeruleus of selective agonists at various opioid receptor subtypes in rats

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