La maladie de Parkinson au Canada (serveur d'exploration)

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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 : 000675 ( PascalFrancis/Curation ); précédent : 000674; suivant : 000676

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 [États-Unis] ; K.-C. Hsieh [États-Unis] ; D. Nguyen [États-Unis] ; J. Peever [Canada] ; J. M. Siegel [États-Unis]

Source :

RBID : Pascal:08-0364351

Descripteurs français

English descriptors

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.
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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
A11 01  1    @1 LAI (Y.-Y.)
A11 02  1    @1 HSIEH (K.-C.)
A11 03  1    @1 NGUYEN (D.)
A11 04  1    @1 PEEVER (J.)
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.
A20       @1 431-443
A21       @1 2008
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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  FRE  @0 Lésion @5 01
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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
C03 02  X  SPA  @0 Sueño paradojal @5 02
C03 03  X  FRE  @0 Muscle @5 03
C03 03  X  ENG  @0 Muscle @5 03
C03 03  X  SPA  @0 Músculo @5 03
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C03 05  X  FRE  @0 Membre inférieur @5 05
C03 05  X  ENG  @0 Lower limb @5 05
C03 05  X  SPA  @0 Miembro inferior @5 05
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C03 06  X  SPA  @0 Conducta @5 06
C03 07  X  FRE  @0 Locus niger @5 07
C03 07  X  ENG  @0 Locus niger @5 07
C03 07  X  SPA  @0 Locus níger @5 07
C03 08  X  FRE  @0 Maladie de Parkinson @2 NM @5 09
C03 08  X  ENG  @0 Parkinson disease @2 NM @5 09
C03 08  X  SPA  @0 Parkinson enfermedad @2 NM @5 09
C07 01  X  FRE  @0 Maladie dégénérative @5 20
C07 01  X  ENG  @0 Degenerative disease @5 20
C07 01  X  SPA  @0 Enfermedad degenerativa @5 20
C07 02  X  FRE  @0 Pathologie du système nerveux @5 21
C07 02  X  ENG  @0 Nervous system diseases @5 21
C07 02  X  SPA  @0 Sistema nervioso patología @5 21
C07 03  X  FRE  @0 Pathologie de l'encéphale @5 22
C07 03  X  ENG  @0 Cerebral disorder @5 22
C07 03  X  SPA  @0 Encéfalo patología @5 22
C07 04  X  FRE  @0 Syndrome extrapyramidal @5 23
C07 04  X  ENG  @0 Extrapyramidal syndrome @5 23
C07 04  X  SPA  @0 Extrapiramidal síndrome @5 23
C07 05  X  FRE  @0 Pathologie du système nerveux central @5 24
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C07 06  X  FRE  @0 Encéphale @5 25
C07 06  X  ENG  @0 Encephalon @5 25
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N21       @1 231
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<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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<s0>Sommeil paradoxal</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Rapid eye movement sleep</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Sueño paradojal</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Muscle</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Muscle</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Músculo</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Modèle animal</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Animal model</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Modelo animal</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Membre inférieur</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Lower limb</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Miembro inferior</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE">
<s0>Comportement</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG">
<s0>Behavior</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA">
<s0>Conducta</s0>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE">
<s0>Locus niger</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG">
<s0>Locus niger</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA">
<s0>Locus níger</s0>
<s5>07</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE">
<s0>Maladie de Parkinson</s0>
<s2>NM</s2>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG">
<s0>Parkinson disease</s0>
<s2>NM</s2>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA">
<s0>Parkinson enfermedad</s0>
<s2>NM</s2>
<s5>09</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>20</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>20</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>20</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Pathologie du système nerveux</s0>
<s5>21</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>21</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>21</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Pathologie de l'encéphale</s0>
<s5>22</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>22</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>22</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Syndrome extrapyramidal</s0>
<s5>23</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>23</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>23</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Pathologie du système nerveux central</s0>
<s5>24</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>24</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>24</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Encéphale</s0>
<s5>25</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Encephalon</s0>
<s5>25</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Encéfalo</s0>
<s5>25</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Système nerveux central</s0>
<s5>26</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Central nervous system</s0>
<s5>26</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Sistema nervioso central</s0>
<s5>26</s5>
</fC07>
<fN21>
<s1>231</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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