Role of medullary reticular neurons in the inhibition of trigeminal motoneurons during active sleep

Chase, Michael H.; Enomoto, S.; Hiraba, Katsunari; Katoh, M.; Nakamura, Yoshio; Sahara, Yoshinori; Taira, Masato

doi:10.1016/0014-4886(84)90233-4

Cited by 34 publications

(13 citation statements)

References 24 publications

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“…These glycinergic/GABAergic VMM neurons, as discussed below, are located just rostral to the inferior olive in the ventral gigantocellular reticular (GiV) and the alpha gigantocellular reticular (GiA) nuclei (Luppi et al, 2012). In support of this idea, single unit recordings demonstrate that the VMM contains neurons that fire fastest in REM sleep, slower in NREM sleep, and very little during wake, correlating with the amount of muscle atonia (Chase et al, 1984). Furthermore, VMM lesions partially disrupt the atonia of REM sleep (Holmes and Jones, 1994; Schenkel and Siegel, 1989).…”

Section: Regulation Of Rem Sleepmentioning

confidence: 93%

Neural Circuitry of Wakefulness and Sleep

Scammell

Arrigoni

Lipton

2017

Neuron

725

616

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SUMMARY Sleep remains one of the most mysterious yet ubiquitous animal behaviors. We review current perspectives on the neural systems that regulate sleep/wake states in mammals and the circadian mechanisms that control their timing. We also outline key models for the regulation of rapid eye movement (REM) sleep and non-REM sleep, how mutual inhibition between specific pathways gives rise to these distinct states, and how dysfunction in these circuits can give rise to sleep disorders.

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Section: Regulation Of Rem Sleepmentioning

confidence: 93%

Neural Circuitry of Wakefulness and Sleep

Scammell

Arrigoni

Lipton

2017

Neuron

725

616

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“…Electrical stimulation of this region suggested the existence of a direct, monosynaptic inhibitory projection from this region to masseter motoneurons (Nakamura et al, 1975). In addition, Chase et al (1984) recorded units in this region that showed their highest frequency of discharge during AS and elicited monosynaptic I PSPs in the masseter pool as determined by field potential analysis using spike-triggered averaging techniques.…”

Section: The Reticular Formation Subdivisions Populated By Double-labmentioning

confidence: 92%

“…Glutamatergic stimulation suppresses the tone of the cervical musculature in the decerebrate cat, an effect that is viewed by the authors Siegel, 1988, 1990) as reflecting the process by which the atonia of AS is generated. Extracellular recordings from NRGc and Mc neurons demonstrate units that discharge specifically during AS (Kanamori et al, 1980;Chase et al, 1984;Sakai, 1988). In narcoleptic dogs specific discharge of Mc units has been described during cataplectic attacks (Siegel et al, 1991).…”

Section: The Reticular Formation Subdivisions Populated By Double-labmentioning

confidence: 96%

c-fosExpression in Brainstem Premotor Interneurons during Cholinergically Induced Active Sleep in the Cat

et al. 1999

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The present study was undertaken to identify trigeminal premotor interneurons that become activated during carbachol-induced active sleep (c-AS). Their identification is a critical step in determining the neural circuits responsible for the atonia of active sleep. Accordingly, the retrograde tracer cholera toxin subunit B (CTb) was injected into the trigeminal motor nuclei complex to label trigeminal interneurons. To identify retrograde-labeled activated neurons, immunocytochemical techniques, designed to label the Fos protein, were used. Double-labeled (i.e., CTb(+), Fos(+)) neurons were found exclusively in the ventral portion of the medullary reticular formation, medial to the facial motor nucleus and lateral to the inferior olive. This region, which encompasses the ventral portion of the nucleus reticularis gigantocellularis and the nucleus magnocellularis, corresponds to the rostral portion of the classic inhibitory region of. This region contained a mean of 606 +/- 41.5 ipsilateral and 90 +/- 32.0 contralateral, CTb-labeled neurons. These cells were of medium-size with an average soma diameter of 20-35 micrometer. Approximately 55% of the retrogradely labeled cells expressed c-fos during a prolonged episode of c-AS. We propose that these neurons are the interneurons responsible for the nonreciprocal postsynaptic inhibition of trigeminal motoneurons that occurs during active sleep.

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“…Within the dorsolateral pons, REM-active glutamatergic cells in the sublaterodorsal nucleus (SLD) in rats and mice project directly to the ventral horn of the spinal cord and mediate REM sleep atonia (Lu et al, 2006; Krenzer et al, 2011). The ventral medulla, on the other hand, contains more diffuse cell populations that regulate atonia through direct projections to the spinal cord and other motoneuron populations (Chase et al, 1984; Holmes and Jones, 1994). Ultimately, it is the hyperpolarization of motoneurons during REM sleep (Nakamura et al, 1978) that produces atonia, with the inhibitory drive deriving from glycinergic inhibitory post-synaptic potentials (Chase et al, 1989; Chase and Morales, 1990) at the level of the spinal cord ventral horn, although some motor systems may have alternative inhibitory mechanisms (Morrison et al, 2003; Brooks and Peever, 2008).…”

Section: Introductionmentioning

confidence: 99%

Ventral medullary control of rapid eye movement sleep and atonia

Chen

Vetrivelan

Guo

et al. 2017

Experimental Neurology

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Discrete populations of neurons at multiple levels of the brainstem control rapid eye movement (REM) sleep and the accompanying loss of postural muscle tone, or atonia. The specific contributions of these brainstem cell populations to REM sleep control remains incompletely understood. Here we show in rats that viral vector-based lesions of the ventromedial medulla at a level rostral to the inferior olive (pSOM) produced violent myoclonic twitches and abnormal electromyographic spikes, but not complete loss of tonic atonia, during REM sleep. Motor tone during non-REM (NREM) sleep was unaffected in these same animals. Acute chemogenetic activation of pSOM neurons in rats robustly and selectively suppressed REM sleep but not NREM sleep. Similar lesions targeting the more rostral ventromedial medulla (RVM) did not affect sleep or atonia, while chemogenetic stimulation of the RVM produced wakefulness and reduced sleep. Finally, selective activation of vesicular GABA transporter (VGAT) pSOM neurons in mice produced complete suppression of REM sleep whereas their loss increased EMG spikes during REM sleep. These results reveal a key contribution of the pSOM and specifically the VGAT+ neurons in this region in REM sleep and motor control.

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Role of medullary reticular neurons in the inhibition of trigeminal motoneurons during active sleep

Cited by 34 publications

References 24 publications

Neural Circuitry of Wakefulness and Sleep

Neural Circuitry of Wakefulness and Sleep

c-fosExpression in Brainstem Premotor Interneurons during Cholinergically Induced Active Sleep in the Cat

Ventral medullary control of rapid eye movement sleep and atonia

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