Different behaviors during paradoxical sleep without atonia depend on pontine lesion site

Hendricks, Joan C.; Morrison, Adrian R.; Mann, Graziella L.

doi:10.1016/0006-8993(82)90835-6

Cited by 357 publications

(140 citation statements)

References 25 publications

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“…Although previous animal studies identify brainstem circuits underlying abnormal REM motor control (Jouvet and Delorme, 1965;Hendricks et al, 1982;Friedman and Jones, 1984;Schenkel and Siegel, 1989;Shouse and Siegel, 1992;Holmes and Jones, 1994;Sanford et al, 2001;Lu et al, 2006;Vetrivelan et al, 2009), this new model represents an important advance because it recapitulates all primary RBD features stemming from a defined genetic mutation. We propose that these transgenic mice are a useful model for determining how glycine and GABA contribute to RBD symptoms.…”

Section: A Mouse Model Of Rbdmentioning

confidence: 96%

Impaired GABA and Glycine Transmission Triggers Cardinal Features of Rapid Eye Movement Sleep Behavior Disorder in Mice

Brooks¹,

Peever²

2011

J. Neurosci.

116

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Rapid eye movement (REM) sleep behavior disorder (RBD) is a neurological disease characterized by loss of normal REM motor inhibition and subsequent dream enactment. RBD is clinically relevant because it predicts neurodegenerative disease onset (e.g., Parkinson's disease) and is clinically problematic because it disrupts sleep and results in patient injuries and hospitalization. Even though the cause of RBD is unknown, multiple lines of evidence indicate that abnormal inhibitory transmission underlies the disorder. Here, we show that transgenic mice with deficient glycine and GABA transmission have a behavioral, motor, and sleep phenotype that recapitulates the cardinal features of RBD. Specifically, we show that mice with impaired glycine and GABA A receptor function exhibit REM motor behaviors, non-REM muscle twitches, sleep disruption, and EEG slowing-the defining disease features. Importantly, the RBD phenotype is rescued by drugs (e.g., clonazepam and melatonin) that are routinely used to treat human disease symptoms. Our findings are the first to identify a potential mechanism for RBD-we show that deficits in glycine-and GABA A -mediated inhibition trigger the full spectrum of RBD symptoms. We propose that these mice are a useful resource for investigating in vivo disease mechanisms and developing potential therapeutics for RBD.

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Section: A Mouse Model Of Rbdmentioning

confidence: 96%

Impaired GABA and Glycine Transmission Triggers Cardinal Features of Rapid Eye Movement Sleep Behavior Disorder in Mice

Brooks¹,

Peever²

2011

J. Neurosci.

116

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“…A higher limbic activity in a normal REM sleep period may thus preferentially excite this system, and result in muscular atonia. However experimental lesions in the muscle tone inhibitory system, such as the PRF (Hendricks et al, 1982) and the medial MRF (Schenkel and Siegel, 1989), have induced "REM without atonia", which is an animal model of human RBD. Signals through the limbic system may preferentially activate the excitatory system and rhythm generating system via the MLR if motor inhibition is insufficient (Takakusaki et al, 2006).…”

Section: Implications Of Pathophysiological Mechanisms Of Narcolepsymentioning

confidence: 99%

Forebrain control of locomotor behaviors

Takakusaki

2008

Brain Research Reviews

133

120

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Activation of different areas in the forebrain evokes different types of goal directed adaptive behaviors. An important component of these different patterns of behavior is the locomotion that brings the animal to or away from a particular location.Here I review the role of projections from forebrain structures to the mesopontine tegmentum of the brainstem where neural mechanisms for initiation of locomotion and regulation of postural muscle tone are located that are activated during locomotor behavior. It is interesting is to understand how signals that converge from the forebrain structures to the mesopontine tegmentum control locomotor behavior, because the mesopontine tegmentum receives inhibitory efferents from the basal ganglia and excitatory efferents from the limbic-hypothalamic system and the neocortex. Here I hypothesize that the mesopontine tegmentum has functional gating mechanisms that determine whether the subject will initiate and select volitionally-guided or emotionally-triggered locomotor behaviors, depending on the behavioral context.

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“…The pathology could be similar to that of the experimental lesions in cats that have produced REM sleep without atonia. Experimentally, lesions of the PRF (Hendricks et al, 1982) and the medial part of the MRF (Schenkel and Siegel, 1989) in cats have produced REM sleep without atonia which is called "dream enactment" (Morrison, 1983). One of the mechanisms of the "REM without atonia" is schematically shown in Fig.…”

Section: -2 Pathophysiology Of Rbdmentioning

confidence: 99%

Neurobiological basis of state-dependent control of motor behaviors

Takakusaki

Saitoh

Nonaka³

et al. 2006

Sleep and Biological Rhythms

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We note the importance of an appropriate combination of excitability for the higher (neocortex, basal ganglia, and limbic system) and lower (brainstem-spinal cord) motor systems could be necessary for normal behavior during wakefulness and REM sleep.Neurotransmitters such as acetylcholine, the monoamines, GABA, and the orexins, would regulate the background excitability of the higher and lower motor systems so that an interaction of these systems could be appropriately maintained. Pathophysiological mechanisms of sleep deficiency may be induced by not only an organic disturbance of brain structures (hardware) but also by dysfunction of the neurotransmitter systems (software). From these considerations, we provide a hypothetical model for "state-dependent interaction of the higher and lower motor systems" for understanding normal behavior and pathophysiological mechanisms of sleep-related disorders such as narcolepsy and the REM-sleep behavioral syndrome.2

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Different behaviors during paradoxical sleep without atonia depend on pontine lesion site

Cited by 357 publications

References 25 publications

Impaired GABA and Glycine Transmission Triggers Cardinal Features of Rapid Eye Movement Sleep Behavior Disorder in Mice

Impaired GABA and Glycine Transmission Triggers Cardinal Features of Rapid Eye Movement Sleep Behavior Disorder in Mice

Forebrain control of locomotor behaviors

Neurobiological basis of state-dependent control of motor behaviors

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