Induction of rapid eye movement sleep by carbachol infusion into the pontine reticular formation in the rat

Bourgin, Patrice; Escourrou, P.; Gaultier, Claude; Adrien, Joëlle

doi:10.1097/00001756-199502000-00031

Cited by 140 publications

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“…Because of the stimulatory effect of UII on PPT neurons, it is likely that UII induces acetylcholine release in the pontine reticular formation and induces REM sleep. The magnitude of the increase in REM recorded in this study is at least as large as that recorded when carbachol is injected into the oral pontine reticular nucleus of the rat, which induces an increase in REM sleep episodes with no change in episode length or latency to REM onset (Bourgin et al, 1995). Microinjection of carbachol into the medial gigantocellular tegmental field produces an increase in ACh release for 7 h that has been related to .…”

Section: Discussionsupporting

confidence: 57%

“…Previous studies in cats and rats have demonstrated the role of PPT and LDT nuclei in sleep regulation. The injection of cholinergic agonists into the medial pontine reticular formation, a target region of the PPT and LDT, induces a rapid eye movement (REM)-like state (George et al, 1964;Baghdoyan et al, 1984;Quattrochi et al, 1989;Bourgin et al, 1995) including cortical desynchronization, hippocampal theta rhythm, muscle atonia, reduction of REM sleep onset, and increase in total time of REM sleep (Vanni-Mercier et al, 1989;Yamamoto et al, 1990;Vertes et al, 1993). These and other studies (for review, see Steriade and McCarley, 1990) clearly indicate that cholinergic neurons in the PPT are important regulators of REM sleep.…”

Section: Introductionmentioning

confidence: 99%

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Urotensin II Modulates Rapid Eye Movement Sleep through Activation of Brainstem Cholinergic Neurons

Huitrón‐Reséndiz

Kristensen²,

Sanchez‐Alavez³

et al. 2005

Journal of Neuroscience

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Urotensin II (UII) is a cyclic neuropeptide with strong vasoconstrictive activity in the peripheral vasculature. UII receptor mRNA is also expressed in the CNS, in particular in cholinergic neurons located in the mesopontine tegmental area, including the pedunculopontine tegmental (PPT) and lateral dorsal tegmental nuclei. This distribution suggests that the UII system is involved in functions regulated by acetylcholine, such as the sleep-wake cycle. Here, we tested the hypothesis that UII influences cholinergic PPT neuron activity and alters rapid eye movement (REM) sleep patterns in rats. Local administration of UII into the PPT nucleus increases REM sleep without inducing changes in the cortical blood flow. Intracerebroventricular injection of UII enhances both REM sleep and wakefulness and reduces slow-wave sleep 2. Intracerebroventricular, but not local, administration of UII increases cortical blood flow. Moreover, whole-cell recordings from rat-brain slices show that UII selectively excites cholinergic PPT neurons via an inward current and membrane depolarization that were accompanied by membrane conductance decreases. This effect does not depend on action potential generation or fast synaptic transmission because it persisted in the presence of TTX and antagonists of ionotropic glutamate, GABA, and glycine receptors. Collectively, these results suggest that UII plays a role in the regulation of REM sleep independently of its cerebrovascular actions by directly activating cholinergic brainstem neurons.

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Section: Discussionsupporting

confidence: 57%

Section: Introductionmentioning

confidence: 99%

Urotensin II Modulates Rapid Eye Movement Sleep through Activation of Brainstem Cholinergic Neurons

Huitrón‐Reséndiz

Kristensen²,

Sanchez‐Alavez³

et al. 2005

Journal of Neuroscience

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“…Since brainstem acetylcholine neurons projecting to the reticular formation increase their activity levels during REM sleep (reviewed in (McCarley, 2004) we believe that CARB-E SubC reticular neurons are likely to be REM-on (muscle-atonia ON) cells. In the cat, infusion of carbachol into the SubC reliably elicits a REM-like state (Baghdoyan et al, 1987; VanniMercier et al, 1989;Yamamoto et al, 1990) but this effect has been difficult to reproduce in the rat (Gnadt and Pegram, 1986;Bourgin et al, 1995;Deurveilher et al, 1997;Boissard et al, 2002). In contrast, infusion of GABA A receptor antagonists or glutamatergic agonists into the rat SubC did lead to a REM-like state being generated (Boissard et al, 2002 Pollock andMistlberger, 2003).…”

Section: Nih-pa Author Manuscriptmentioning

confidence: 99%

Electrophysiological characterization of neurons in the dorsolateral pontine rapid-eye-movement sleep induction zone of the rat: Intrinsic membrane properties and responses to carbachol and orexins

et al. 2006

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Pharmacological, lesion and single-unit recording techniques in several animal species have identified a region of the pontine reticular formation (Subcoeruleus, SubC) just ventral to the locus coeruleus as critically involved in the generation of rapid-eye-movement (REM) sleep. However, the intrinsic membrane properties and responses of SubC neurons to neurotransmitters important in REM sleep control, such as acetylcholine and orexins/hypocretins, have not previously been examined in any animal species and thus were targeted in this study.We obtained whole-cell patch-clamp recordings from visually identified SubC neurons in rat brain slices in vitro. Two groups of large neurons (mean diameter 30 and 27μm) were tentatively identified as cholinergic (rostral SubC) and noradrenergic (caudal SubC) neurons. SubC reticular neurons (noncholinergic, non-noradrenergic) showed a medium-sized depolarizing sag during hyperpolarizing current pulses and often had a rebound depolarization (low-threshold spike, LTS). During depolarizing current pulses they exhibited little adaptation and fired maximally at 30-90 Hz. Those SubC reticular neurons excited by carbachol (n=27) fired spontaneously at 6 Hz, often exhibited a moderately sized LTS, and varied widely in size (17-42 μm). Carbachol-inhibited SubC reticular neurons were medium-sized (15-25 μm) and constituted two groups. The larger group (n=22) was silent at rest and possessed a prominent LTS and associated 1-4 action potentials. The second, smaller group (n=8) had a delayed return to baseline at the offset of hyperpolarizing pulses. Orexins excited both carbachol excited and carbachol inhibited SubC reticular neurons.SubC reticular neurons had intrinsic membrane properties and responses to carbachol similar to those described for other reticular neurons but a larger number of carbachol inhibited neurons were found (> 50 %), the majority of which demonstrated a prominent LTS and may correspond to PGO-on neurons. Some or all carbachol-excited neurons are presumably REM-on neurons.Keywords rapid-eye-movement; whole-cell; in vitro; sublaterodorsal; hypocretin; narcolepsy NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptAbbreviations ACSF Artificial cerebrospinal fluid; AHP Afterhyperpolarization; AP Action potential; CARB Carbachol; CARB-E Carbachol excited; CARB-I Carbachol inhibited; CCD Charge coupled device; ChAT Choline acetyltransferase; DAB Diaminobenzidine; DC Direct current; GABA Gammaamino-butyric acid; GAD67 glutamic acid decarboxylase 67 kDa isoform; HCN Hyperpolarization activated and cyclic nucleotide gated cation channels; IACUC Institutional Animal Care and Use committee; IR-DIC Infra-red differential interference contrast; LC locus coeruleus; LDT laterodorsal tegmental nucleus; LTS low-threshold spike; mPRF medial pontine reticular formation; nNOS neuronal nitric oxide synthase; Ox A Orexin A; PGO pontine-geniculate-occipital waves; PnC pontine nucleus caudalis; PnO pontine nucleus oralis; P waves Pontine component of PGO wave...

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“…For example, cholinergic stimulation of the PRF in rodents does not reliably enhance REM sleep, inducing wakefulness or having no effect in many cases (Bourgin et al, 1995;Deurveilher et al, 1997;Boissard et al, 2002;Pollock and Mistlberger, 2005), and endogenous acetylcholine in the PRF has not been shown necessary for REM sleep generation as tested by focal application of acetylcho-line receptor antagonists. REM sleep-active PPTn neurons are also predominately noncholinergic (Maloney et al, 1999;Verret et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

5-HT_1AReceptor-Responsive Pedunculopontine Tegmental Neurons Suppress REM Sleep and Respiratory Motor Activity

Grace¹,

Liu²,

Horner³

2012

J. Neurosci.

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Induction of rapid eye movement sleep by carbachol infusion into the pontine reticular formation in the rat

Cited by 140 publications

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Urotensin II Modulates Rapid Eye Movement Sleep through Activation of Brainstem Cholinergic Neurons

Urotensin II Modulates Rapid Eye Movement Sleep through Activation of Brainstem Cholinergic Neurons

Electrophysiological characterization of neurons in the dorsolateral pontine rapid-eye-movement sleep induction zone of the rat: Intrinsic membrane properties and responses to carbachol and orexins

5-HT_1AReceptor-Responsive Pedunculopontine Tegmental Neurons Suppress REM Sleep and Respiratory Motor Activity

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Induction of rapid eye movement sleep by carbachol infusion into the pontine reticular formation in the rat

Cited by 140 publications

References 0 publications

Urotensin II Modulates Rapid Eye Movement Sleep through Activation of Brainstem Cholinergic Neurons

Urotensin II Modulates Rapid Eye Movement Sleep through Activation of Brainstem Cholinergic Neurons

Electrophysiological characterization of neurons in the dorsolateral pontine rapid-eye-movement sleep induction zone of the rat: Intrinsic membrane properties and responses to carbachol and orexins

5-HT1AReceptor-Responsive Pedunculopontine Tegmental Neurons Suppress REM Sleep and Respiratory Motor Activity

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5-HT_1AReceptor-Responsive Pedunculopontine Tegmental Neurons Suppress REM Sleep and Respiratory Motor Activity