ParkinsonCanadaV1, PascalFrancis, Corpus, bibRecord, 000635

NEUROTOXIC LESIONS AT THE VENTRAL MESOPONTINE JUNCTION CHANGE SLEEP TIME AND MUSCLE ACTIVITY DURING SLEEP : AN ANIMAL MODEL OF MOTOR DISORDERS IN SLEEP

Identifieur interne : 000635 ( PascalFrancis/Corpus ); précédent : 000634; suivant : 000636

NEUROTOXIC LESIONS AT THE VENTRAL MESOPONTINE JUNCTION CHANGE SLEEP TIME AND MUSCLE ACTIVITY DURING SLEEP : AN ANIMAL MODEL OF MOTOR DISORDERS IN SLEEP

Auteurs : Y.-Y. Lai ; K.-C. Hsieh ; D. Nguyen ; J. Peever ; J. M. Siegel

Source :

Neuroscience [ 0306-4522 ] ; 2008.

RBID : Pascal:08-0364351

Descripteurs français

Pascal (Inist)
- Lésion, Sommeil paradoxal, Muscle, Modèle animal, Membre inférieur, Comportement, Locus niger, Maladie de Parkinson.

English descriptors

KwdEn :
- Animal model, Behavior, Lesion, Locus niger, Lower limb, Muscle, Parkinson disease, Rapid eye movement sleep.

Abstract

There is no adequate animal model of restless legs syndrome (RLS) and periodic leg movements disorder (PLMD), disorders affecting 10% of the population. Similarly, there is no model of rapid eye movement (REM) sleep behavior disorder (RBD) that explains its symptoms and its link to Parkinsonism. We previously reported that the motor inhibitory system in the brainstem extends from the medulla to the ventral mesopontine junction (VMPJ). We now examine the effects of damage to the VMPJ in the cat. Based on the lesion sites and the changes in sleep pattern and behavior, we saw three distinct syndromes resulting from such lesions; the rostrolateral, rostromedial and caudalVMPJ syndromes. The change in sleep pattern was dependent on the lesion site, but was not significantly correlated with the number of dopaminergic neurons lost. An increase in wakefulness and a decrease in slow wave sleep (SWS) and REM sleep were seen in the rostrolateral VMPJ-lesioned animals. In contrast, the sleep pattern was not significantly changed in the rostromedial and caudal VMPJ-lesioned animals. All three groups of animals showed a significant increase in periodic and isolated leg movements in SWS and increased tonic muscle activity in REM sleep. Beyond these common symptoms, an increase in phasic motor activity in REM sleep, resembling that seen in human RBD, was found in the caudal VMPJ-lesioned animals. In contrast, the increase in motor activity in SWS in rostral VMPJ-lesioned animals is similar to that seen in human RLS/PLMD patients. The proximity of the VMPJ region to the substantia nigra suggests that the link between RLS/PLMD and Parkinsonism, as well as the progression from RBD to Parkinsonism may be mediated by the spread of damage from the regions identified here into the substantia nigra.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A08	`01`	`1`	`ENG`	`@1 NEUROTOXIC LESIONS AT THE VENTRAL MESOPONTINE JUNCTION CHANGE SLEEP TIME AND MUSCLE ACTIVITY DURING SLEEP : AN ANIMAL MODEL OF MOTOR DISORDERS IN SLEEP`
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A11	`05`	`1`		`@1 SIEGEL (J. M.)`
A14	`01`			`@1 Department of Psychiatry and Biobehavioral Science, Neurobiology Research (151A3), David Geffen School of Medicine, UCLA and Veterans Administration Greater Los Angeles Healthcare System Sepulveda, 16111 Plummer Street @2 North Hills, CA 91343 @3 USA @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 5 aut.`
A14	`02`			`@1 Systems Neurobiology Laboratory, Departments of Physiology and Cell and Systems Biology, University of Toronto, 25 Harbord Street @2 Toronto, ON, M5S 3G5 @3 CAN @Z 4 aut.`
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C01	`01`		`ENG`	@0 There is no adequate animal model of restless legs syndrome (RLS) and periodic leg movements disorder (PLMD), disorders affecting 10% of the population. Similarly, there is no model of rapid eye movement (REM) sleep behavior disorder (RBD) that explains its symptoms and its link to Parkinsonism. We previously reported that the motor inhibitory system in the brainstem extends from the medulla to the ventral mesopontine junction (VMPJ). We now examine the effects of damage to the VMPJ in the cat. Based on the lesion sites and the changes in sleep pattern and behavior, we saw three distinct syndromes resulting from such lesions; the rostrolateral, rostromedial and caudalVMPJ syndromes. The change in sleep pattern was dependent on the lesion site, but was not significantly correlated with the number of dopaminergic neurons lost. An increase in wakefulness and a decrease in slow wave sleep (SWS) and REM sleep were seen in the rostrolateral VMPJ-lesioned animals. In contrast, the sleep pattern was not significantly changed in the rostromedial and caudal VMPJ-lesioned animals. All three groups of animals showed a significant increase in periodic and isolated leg movements in SWS and increased tonic muscle activity in REM sleep. Beyond these common symptoms, an increase in phasic motor activity in REM sleep, resembling that seen in human RBD, was found in the caudal VMPJ-lesioned animals. In contrast, the increase in motor activity in SWS in rostral VMPJ-lesioned animals is similar to that seen in human RLS/PLMD patients. The proximity of the VMPJ region to the substantia nigra suggests that the link between RLS/PLMD and Parkinsonism, as well as the progression from RBD to Parkinsonism may be mediated by the spread of damage from the regions identified here into the substantia nigra.
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C03	`01`	`X`	`ENG`	`@0 Lesion @5 01`
C03	`01`	`X`	`SPA`	`@0 Lesión @5 01`
C03	`02`	`X`	`FRE`	`@0 Sommeil paradoxal @5 02`
C03	`02`	`X`	`ENG`	`@0 Rapid eye movement sleep @5 02`
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C03	`03`	`X`	`ENG`	`@0 Muscle @5 03`
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C03	`05`	`X`	`ENG`	`@0 Lower limb @5 05`
C03	`05`	`X`	`SPA`	`@0 Miembro inferior @5 05`
C03	`06`	`X`	`FRE`	`@0 Comportement @5 06`
C03	`06`	`X`	`ENG`	`@0 Behavior @5 06`
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C03	`07`	`X`	`FRE`	`@0 Locus niger @5 07`
C03	`07`	`X`	`ENG`	`@0 Locus niger @5 07`
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C07	`02`	`X`	`FRE`	`@0 Pathologie du système nerveux @5 21`
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C07	`02`	`X`	`SPA`	`@0 Sistema nervioso patología @5 21`
C07	`03`	`X`	`FRE`	`@0 Pathologie de l'encéphale @5 22`
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C07	`04`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 23`
C07	`05`	`X`	`FRE`	`@0 Pathologie du système nerveux central @5 24`
C07	`05`	`X`	`ENG`	`@0 Central nervous system disease @5 24`
C07	`05`	`X`	`SPA`	`@0 Sistema nervosio central patología @5 24`
C07	`06`	`X`	`FRE`	`@0 Encéphale @5 25`
C07	`06`	`X`	`ENG`	`@0 Encephalon @5 25`
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Format Inist (serveur)

NO :	PASCAL 08-0364351 INIST
ET :	NEUROTOXIC LESIONS AT THE VENTRAL MESOPONTINE JUNCTION CHANGE SLEEP TIME AND MUSCLE ACTIVITY DURING SLEEP : AN ANIMAL MODEL OF MOTOR DISORDERS IN SLEEP
AU :	LAI (Y.-Y.); HSIEH (K.-C.); NGUYEN (D.); PEEVER (J.); SIEGEL (J. M.)
AF :	Department of Psychiatry and Biobehavioral Science, Neurobiology Research (151A3), David Geffen School of Medicine, UCLA and Veterans Administration Greater Los Angeles Healthcare System Sepulveda, 16111 Plummer Street/North Hills, CA 91343/Etats-Unis (1 aut., 2 aut., 3 aut., 5 aut.); Systems Neurobiology Laboratory, Departments of Physiology and Cell and Systems Biology, University of Toronto, 25 Harbord Street/Toronto, ON, M5S 3G5/Canada (4 aut.)
DT :	Publication en série; Niveau analytique
SO :	Neuroscience; ISSN 0306-4522; Coden NRSCDN; Royaume-Uni; Da. 2008; Vol. 154; No. 2; Pp. 431-443; Bibl. 2 p.1/4
LA :	Anglais
EA :	There is no adequate animal model of restless legs syndrome (RLS) and periodic leg movements disorder (PLMD), disorders affecting 10% of the population. Similarly, there is no model of rapid eye movement (REM) sleep behavior disorder (RBD) that explains its symptoms and its link to Parkinsonism. We previously reported that the motor inhibitory system in the brainstem extends from the medulla to the ventral mesopontine junction (VMPJ). We now examine the effects of damage to the VMPJ in the cat. Based on the lesion sites and the changes in sleep pattern and behavior, we saw three distinct syndromes resulting from such lesions; the rostrolateral, rostromedial and caudalVMPJ syndromes. The change in sleep pattern was dependent on the lesion site, but was not significantly correlated with the number of dopaminergic neurons lost. An increase in wakefulness and a decrease in slow wave sleep (SWS) and REM sleep were seen in the rostrolateral VMPJ-lesioned animals. In contrast, the sleep pattern was not significantly changed in the rostromedial and caudal VMPJ-lesioned animals. All three groups of animals showed a significant increase in periodic and isolated leg movements in SWS and increased tonic muscle activity in REM sleep. Beyond these common symptoms, an increase in phasic motor activity in REM sleep, resembling that seen in human RBD, was found in the caudal VMPJ-lesioned animals. In contrast, the increase in motor activity in SWS in rostral VMPJ-lesioned animals is similar to that seen in human RLS/PLMD patients. The proximity of the VMPJ region to the substantia nigra suggests that the link between RLS/PLMD and Parkinsonism, as well as the progression from RBD to Parkinsonism may be mediated by the spread of damage from the regions identified here into the substantia nigra.
CC :	002A25K; 002B17G
FD :	Lésion; Sommeil paradoxal; Muscle; Modèle animal; Membre inférieur; Comportement; Locus niger; Maladie de Parkinson
FG :	Maladie dégénérative; Pathologie du système nerveux; Pathologie de l'encéphale; Syndrome extrapyramidal; Pathologie du système nerveux central; Encéphale; Système nerveux central
ED :	Lesion; Rapid eye movement sleep; Muscle; Animal model; Lower limb; Behavior; Locus niger; Parkinson disease
EG :	Degenerative disease; Nervous system diseases; Cerebral disorder; Extrapyramidal syndrome; Central nervous system disease; Encephalon; Central nervous system
SD :	Lesión; Sueño paradojal; Músculo; Modelo animal; Miembro inferior; Conducta; Locus níger; Parkinson enfermedad
LO :	INIST-17194.354000196024820040
ID :	08-0364351

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Pascal:08-0364351

Le document en format XML

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<front><div type="abstract" xml:lang="en">There is no adequate animal model of restless legs syndrome (RLS) and periodic leg movements disorder (PLMD), disorders affecting 10% of the population. Similarly, there is no model of rapid eye movement (REM) sleep behavior disorder (RBD) that explains its symptoms and its link to Parkinsonism. We previously reported that the motor inhibitory system in the brainstem extends from the medulla to the ventral mesopontine junction (VMPJ). We now examine the effects of damage to the VMPJ in the cat. Based on the lesion sites and the changes in sleep pattern and behavior, we saw three distinct syndromes resulting from such lesions; the rostrolateral, rostromedial and caudalVMPJ syndromes. The change in sleep pattern was dependent on the lesion site, but was not significantly correlated with the number of dopaminergic neurons lost. An increase in wakefulness and a decrease in slow wave sleep (SWS) and REM sleep were seen in the rostrolateral VMPJ-lesioned animals. In contrast, the sleep pattern was not significantly changed in the rostromedial and caudal VMPJ-lesioned animals. All three groups of animals showed a significant increase in periodic and isolated leg movements in SWS and increased tonic muscle activity in REM sleep. Beyond these common symptoms, an increase in phasic motor activity in REM sleep, resembling that seen in human RBD, was found in the caudal VMPJ-lesioned animals. In contrast, the increase in motor activity in SWS in rostral VMPJ-lesioned animals is similar to that seen in human RLS/PLMD patients. The proximity of the VMPJ region to the substantia nigra suggests that the link between RLS/PLMD and Parkinsonism, as well as the progression from RBD to Parkinsonism may be mediated by the spread of damage from the regions identified here into the substantia nigra.</div>
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<fA14 i1="02"><s1>Systems Neurobiology Laboratory, Departments of Physiology and Cell and Systems Biology, University of Toronto, 25 Harbord Street</s1>
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<server><NO>PASCAL 08-0364351 INIST</NO>
<ET>NEUROTOXIC LESIONS AT THE VENTRAL MESOPONTINE JUNCTION CHANGE SLEEP TIME AND MUSCLE ACTIVITY DURING SLEEP : AN ANIMAL MODEL OF MOTOR DISORDERS IN SLEEP</ET>
<AU>LAI (Y.-Y.); HSIEH (K.-C.); NGUYEN (D.); PEEVER (J.); SIEGEL (J. M.)</AU>
<AF>Department of Psychiatry and Biobehavioral Science, Neurobiology Research (151A3), David Geffen School of Medicine, UCLA and Veterans Administration Greater Los Angeles Healthcare System Sepulveda, 16111 Plummer Street/North Hills, CA 91343/Etats-Unis (1 aut., 2 aut., 3 aut., 5 aut.); Systems Neurobiology Laboratory, Departments of Physiology and Cell and Systems Biology, University of Toronto, 25 Harbord Street/Toronto, ON, M5S 3G5/Canada (4 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Neuroscience; ISSN 0306-4522; Coden NRSCDN; Royaume-Uni; Da. 2008; Vol. 154; No. 2; Pp. 431-443; Bibl. 2 p.1/4</SO>
<LA>Anglais</LA>
<EA>There is no adequate animal model of restless legs syndrome (RLS) and periodic leg movements disorder (PLMD), disorders affecting 10% of the population. Similarly, there is no model of rapid eye movement (REM) sleep behavior disorder (RBD) that explains its symptoms and its link to Parkinsonism. We previously reported that the motor inhibitory system in the brainstem extends from the medulla to the ventral mesopontine junction (VMPJ). We now examine the effects of damage to the VMPJ in the cat. Based on the lesion sites and the changes in sleep pattern and behavior, we saw three distinct syndromes resulting from such lesions; the rostrolateral, rostromedial and caudalVMPJ syndromes. The change in sleep pattern was dependent on the lesion site, but was not significantly correlated with the number of dopaminergic neurons lost. An increase in wakefulness and a decrease in slow wave sleep (SWS) and REM sleep were seen in the rostrolateral VMPJ-lesioned animals. In contrast, the sleep pattern was not significantly changed in the rostromedial and caudal VMPJ-lesioned animals. All three groups of animals showed a significant increase in periodic and isolated leg movements in SWS and increased tonic muscle activity in REM sleep. Beyond these common symptoms, an increase in phasic motor activity in REM sleep, resembling that seen in human RBD, was found in the caudal VMPJ-lesioned animals. In contrast, the increase in motor activity in SWS in rostral VMPJ-lesioned animals is similar to that seen in human RLS/PLMD patients. The proximity of the VMPJ region to the substantia nigra suggests that the link between RLS/PLMD and Parkinsonism, as well as the progression from RBD to Parkinsonism may be mediated by the spread of damage from the regions identified here into the substantia nigra.</EA>
<CC>002A25K; 002B17G</CC>
<FD>Lésion; Sommeil paradoxal; Muscle; Modèle animal; Membre inférieur; Comportement; Locus niger; Maladie de Parkinson</FD>
<FG>Maladie dégénérative; Pathologie du système nerveux; Pathologie de l'encéphale; Syndrome extrapyramidal; Pathologie du   système nerveux central; Encéphale; Système nerveux central</FG>
<ED>Lesion; Rapid eye movement sleep; Muscle; Animal model; Lower limb; Behavior; Locus niger; Parkinson disease</ED>
<EG>Degenerative disease; Nervous system diseases; Cerebral disorder; Extrapyramidal syndrome; Central nervous system disease; Encephalon; Central nervous system</EG>
<SD>Lesión; Sueño paradojal; Músculo; Modelo animal; Miembro inferior; Conducta; Locus níger; Parkinson enfermedad</SD>
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	La maladie de Parkinson au Canada (serveur d'exploration)
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La maladie de Parkinson au Canada (serveur d'exploration)

NEUROTOXIC LESIONS AT THE VENTRAL MESOPONTINE JUNCTION CHANGE SLEEP TIME AND MUSCLE ACTIVITY DURING SLEEP : AN ANIMAL MODEL OF MOTOR DISORDERS IN SLEEP

NEUROTOXIC LESIONS AT THE VENTRAL MESOPONTINE JUNCTION CHANGE SLEEP TIME AND MUSCLE ACTIVITY DURING SLEEP : AN ANIMAL MODEL OF MOTOR DISORDERS IN SLEEP

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