The neuronal network responsible for paradoxical sleep and its dysfunctions causing narcolepsy and rapid eye movement (REM) behavior disorder.
Identifieur interne : 000930 ( PubMed/Curation ); précédent : 000929; suivant : 000931The neuronal network responsible for paradoxical sleep and its dysfunctions causing narcolepsy and rapid eye movement (REM) behavior disorder.
Auteurs : Pierre-Hervé Luppi [France] ; Olivier Clément ; Emilie Sapin ; Damien Gervasoni ; Christelle Peyron ; Lucienne Léger ; Denise Salvert ; Patrice FortSource :
- Sleep medicine reviews [ 1532-2955 ] ; 2011.
English descriptors
- KwdEn :
- Amygdala (physiopathology), Animals, Brain (physiopathology), Brain Mapping, Cataplexy (physiopathology), Emotions (physiology), Glutamine (physiology), Glycine (physiology), Humans, Hypothalamus (physiopathology), Medulla Oblongata (physiopathology), Motor Neurons (physiology), Muscle Tonus (physiology), Narcolepsy (physiopathology), Nerve Net (physiopathology), Neurodegenerative Diseases (physiopathology), Neurons (physiology), Parkinson Disease (physiopathology), Pedunculopontine Tegmental Nucleus (physiopathology), Pons (physiopathology), REM Sleep Behavior Disorder (physiopathology), Sleep, REM (physiology), Wakefulness (physiology), gamma-Aminobutyric Acid (physiology).
- MESH :
- chemical , physiology : Glutamine, Glycine, gamma-Aminobutyric Acid.
- physiology : Emotions, Motor Neurons, Muscle Tonus, Neurons, Sleep, REM, Wakefulness.
- physiopathology : Amygdala, Brain, Cataplexy, Hypothalamus, Medulla Oblongata, Narcolepsy, Nerve Net, Neurodegenerative Diseases, Parkinson Disease, Pedunculopontine Tegmental Nucleus, Pons, REM Sleep Behavior Disorder.
- Animals, Brain Mapping, Humans.
Abstract
Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by the loss of muscle atonia during paradoxical (REM) sleep (PS). Conversely, cataplexy, one of the key symptoms of narcolepsy, is a striking sudden episode of muscle weakness triggered by emotions during wakefulness, and comparable to REM sleep atonia. The neuronal dysfunctions responsible for RBD and cataplexy are not known. In the present review, we present the most recent results on the neuronal network responsible for PS. Based on these results, we propose an updated integrated model of the mechanisms responsible for PS and explore different hypotheses explaining RBD and cataplexy. We propose that RBD is due to a specific degeneration of a sub-population of PS-on glutamatergic neurons specifically responsible of muscle atonia, localized in the caudal pontine sublaterodorsal tegmental nucleus (SLD). Another possibility is the occurrence in RBD patients of a specific lesion of the glycinergic/GABAergic pre-motoneurons localized in the medullary ventral gigantocellular reticular nucleus. Conversely, cataplexy in narcoleptics would be due to the activation during waking of the caudal PS-on SLD neurons responsible for muscle atonia. A phasic glutamatergic excitatory pathway from the central amygdala to the SLD PS-on neurons activated during emotion would induce such activation. In normal conditions, the glutamate excitation would be blocked by the simultaneous excitation by the hypocretins of the PS-off GABAergic neurons localized in the ventrolateral periaqueductal gray and the adjacent deep mesencephalic reticular nucleus, gating the activation of the PS-on SLD neurons.
DOI: 10.1016/j.smrv.2010.08.002
PubMed: 21115377
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Salvert</name></author><author><name sortKey="Fort, Patrice" sort="Fort, Patrice" uniqKey="Fort P" first="Patrice" last="Fort">Patrice Fort</name></author></analytic><series><title level="j">Sleep medicine reviews</title><idno type="eISSN">1532-2955</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amygdala (physiopathology)</term><term>Animals</term><term>Brain (physiopathology)</term><term>Brain Mapping</term><term>Cataplexy (physiopathology)</term><term>Emotions (physiology)</term><term>Glutamine (physiology)</term><term>Glycine (physiology)</term><term>Humans</term><term>Hypothalamus (physiopathology)</term><term>Medulla Oblongata (physiopathology)</term><term>Motor Neurons (physiology)</term><term>Muscle Tonus (physiology)</term><term>Narcolepsy (physiopathology)</term><term>Nerve Net (physiopathology)</term><term>Neurodegenerative Diseases (physiopathology)</term><term>Neurons (physiology)</term><term>Parkinson Disease (physiopathology)</term><term>Pedunculopontine Tegmental Nucleus (physiopathology)</term><term>Pons (physiopathology)</term><term>REM Sleep Behavior Disorder (physiopathology)</term><term>Sleep, REM (physiology)</term><term>Wakefulness (physiology)</term><term>gamma-Aminobutyric Acid (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Glutamine</term><term>Glycine</term><term>gamma-Aminobutyric Acid</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Emotions</term><term>Motor Neurons</term><term>Muscle Tonus</term><term>Neurons</term><term>Sleep, REM</term><term>Wakefulness</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Amygdala</term><term>Brain</term><term>Cataplexy</term><term>Hypothalamus</term><term>Medulla Oblongata</term><term>Narcolepsy</term><term>Nerve Net</term><term>Neurodegenerative Diseases</term><term>Parkinson Disease</term><term>Pedunculopontine Tegmental Nucleus</term><term>Pons</term><term>REM Sleep Behavior Disorder</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Brain Mapping</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by the loss of muscle atonia during paradoxical (REM) sleep (PS). Conversely, cataplexy, one of the key symptoms of narcolepsy, is a striking sudden episode of muscle weakness triggered by emotions during wakefulness, and comparable to REM sleep atonia. The neuronal dysfunctions responsible for RBD and cataplexy are not known. In the present review, we present the most recent results on the neuronal network responsible for PS. Based on these results, we propose an updated integrated model of the mechanisms responsible for PS and explore different hypotheses explaining RBD and cataplexy. We propose that RBD is due to a specific degeneration of a sub-population of PS-on glutamatergic neurons specifically responsible of muscle atonia, localized in the caudal pontine sublaterodorsal tegmental nucleus (SLD). Another possibility is the occurrence in RBD patients of a specific lesion of the glycinergic/GABAergic pre-motoneurons localized in the medullary ventral gigantocellular reticular nucleus. Conversely, cataplexy in narcoleptics would be due to the activation during waking of the caudal PS-on SLD neurons responsible for muscle atonia. A phasic glutamatergic excitatory pathway from the central amygdala to the SLD PS-on neurons activated during emotion would induce such activation. In normal conditions, the glutamate excitation would be blocked by the simultaneous excitation by the hypocretins of the PS-off GABAergic neurons localized in the ventrolateral periaqueductal gray and the adjacent deep mesencephalic reticular nucleus, gating the activation of the PS-on SLD neurons.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21115377</PMID><DateCreated><Year>2011</Year><Month>04</Month><Day>25</Day></DateCreated><DateCompleted><Year>2011</Year><Month>09</Month><Day>08</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1532-2955</ISSN><JournalIssue CitedMedium="Internet"><Volume>15</Volume><Issue>3</Issue><PubDate><Year>2011</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Sleep medicine reviews</Title><ISOAbbreviation>Sleep Med Rev</ISOAbbreviation></Journal><ArticleTitle>The neuronal network responsible for paradoxical sleep and its dysfunctions causing narcolepsy and rapid eye movement (REM) behavior disorder.</ArticleTitle><Pagination><MedlinePgn>153-63</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.smrv.2010.08.002</ELocationID><Abstract><AbstractText>Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by the loss of muscle atonia during paradoxical (REM) sleep (PS). Conversely, cataplexy, one of the key symptoms of narcolepsy, is a striking sudden episode of muscle weakness triggered by emotions during wakefulness, and comparable to REM sleep atonia. The neuronal dysfunctions responsible for RBD and cataplexy are not known. In the present review, we present the most recent results on the neuronal network responsible for PS. Based on these results, we propose an updated integrated model of the mechanisms responsible for PS and explore different hypotheses explaining RBD and cataplexy. We propose that RBD is due to a specific degeneration of a sub-population of PS-on glutamatergic neurons specifically responsible of muscle atonia, localized in the caudal pontine sublaterodorsal tegmental nucleus (SLD). Another possibility is the occurrence in RBD patients of a specific lesion of the glycinergic/GABAergic pre-motoneurons localized in the medullary ventral gigantocellular reticular nucleus. Conversely, cataplexy in narcoleptics would be due to the activation during waking of the caudal PS-on SLD neurons responsible for muscle atonia. A phasic glutamatergic excitatory pathway from the central amygdala to the SLD PS-on neurons activated during emotion would induce such activation. In normal conditions, the glutamate excitation would be blocked by the simultaneous excitation by the hypocretins of the PS-off GABAergic neurons localized in the ventrolateral periaqueductal gray and the adjacent deep mesencephalic reticular nucleus, gating the activation of the PS-on SLD neurons.</AbstractText><CopyrightInformation>Copyright © 2010 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Luppi</LastName><ForeName>Pierre-Hervé</ForeName><Initials>PH</Initials><AffiliationInfo><Affiliation>UMR5167 CNRS, Institut Fédératif des Neurosciences de Lyon (IFR 19), Univ Lyon 1, Université de Lyon, Lyon, France. luppi@sommeil.univ-lyon1.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Clément</LastName><ForeName>Olivier</ForeName><Initials>O</Initials></Author><Author ValidYN="Y"><LastName>Sapin</LastName><ForeName>Emilie</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Gervasoni</LastName><ForeName>Damien</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Peyron</LastName><ForeName>Christelle</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Léger</LastName><ForeName>Lucienne</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Salvert</LastName><ForeName>Denise</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Fort</LastName><ForeName>Patrice</ForeName><Initials>P</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2010</Year><Month>11</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Sleep Med Rev</MedlineTA><NlmUniqueID>9804678</NlmUniqueID><ISSNLinking>1087-0792</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0RH81L854J</RegistryNumber><NameOfSubstance UI="D005973">Glutamine</NameOfSubstance></Chemical><Chemical><RegistryNumber>56-12-2</RegistryNumber><NameOfSubstance UI="D005680">gamma-Aminobutyric 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