Pallidal gap junctions-triggers of synchrony in Parkinson's disease?
Identifieur interne : 000489 ( Main/Exploration ); précédent : 000488; suivant : 000490Pallidal gap junctions-triggers of synchrony in Parkinson's disease?
Auteurs : Bettina C. Schwab [Pays-Bas] ; Tjitske Heida [Pays-Bas] ; Yan Zhao [Pays-Bas] ; Stephan A. Van Gils [Pays-Bas] ; Richard J A. Van Wezel [Pays-Bas]Source :
- Movement Disorders [ 0885-3185 ] ; 2014.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Basal Ganglia (metabolism), Basal Ganglia (pathology), Computer Simulation, Connexins (metabolism), Female, Gap Junctions (physiology), Globus Pallidus (metabolism), Globus Pallidus (pathology), Glutamate Decarboxylase (metabolism), Humans, Male, Microscopy, Confocal, Models, Neurological, Parkinson Disease (pathology).
- MESH :
- chemical , metabolism : Connexins, Glutamate Decarboxylase.
- metabolism : Basal Ganglia, Globus Pallidus.
- pathology : Basal Ganglia, Globus Pallidus, Parkinson Disease.
- physiology : Gap Junctions.
- Aged, Aged, 80 and over, Computer Simulation, Female, Humans, Male, Microscopy, Confocal, Models, Neurological.
Abstract
Although increased synchrony of the neural activity in the basal ganglia may underlie the motor deficiencies exhibited in Parkinson's disease (PD), how this synchrony arises, propagates through the basal ganglia, and changes under dopamine replacement remains unknown. Gap junctions could play a major role in modifying this synchrony, because they show functional plasticity under the influence of dopamine and after neural injury. In this study, confocal imaging was used to detect connexin-36, the major neural gap junction protein, in postmortem tissues of PD patients and control subjects in the putamen, subthalamic nucleus (STN), and external and internal globus pallidus (GPe and GPi, respectively). Moreover, we quantified how gap junctions affect synchrony in an existing computational model of the basal ganglia. We detected connexin-36 in the human putamen, GPe, and GPi, but not in the STN. Furthermore, we found that the number of connexin-36 spots in PD tissues increased by 50% in the putamen, 43% in the GPe, and 109% in the GPi compared with controls. In the computational model, gap junctions in the GPe and GPi strongly influenced synchrony. The basal ganglia became especially susceptible to synchronize with input from the cortex when gap junctions were numerous and high in conductance. In conclusion, connexin-36 expression in the human GPe and GPi suggests that gap junctional coupling exists within these nuclei. In PD, neural injury and dopamine depletion could increase this coupling. Therefore, we propose that gap junctions act as a powerful modulator of synchrony in the basal ganglia.
Url:
DOI: 10.1002/mds.25987
PubMed: 25124148
PubMed Central: 4307646
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Pallidal gap junctions-triggers of synchrony in Parkinson's disease?</title><author><name sortKey="Schwab, Bettina C" sort="Schwab, Bettina C" uniqKey="Schwab B" first="Bettina C" last="Schwab">Bettina C. Schwab</name><affiliation wicri:level="1"><nlm:aff id="au1"><institution>Applied Analysis, MIRA Institute of Technical Medicine and Biomedical Technology, University of Twente</institution><addr-line>Enschede, The Netherlands</addr-line></nlm:aff><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Enschede</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="au2"><institution>Biomedical Signals and Systems, MIRA Institute of Technical Medicine and Biomedical Technology, University of Twente</institution><addr-line>Enschede, The Netherlands</addr-line></nlm:aff><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Enschede</wicri:regionArea></affiliation></author><author><name sortKey="Heida, Tjitske" sort="Heida, Tjitske" uniqKey="Heida T" first="Tjitske" last="Heida">Tjitske Heida</name><affiliation wicri:level="1"><nlm:aff id="au2"><institution>Biomedical Signals and Systems, MIRA Institute of Technical Medicine and Biomedical Technology, University of Twente</institution><addr-line>Enschede, The Netherlands</addr-line></nlm:aff><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Enschede</wicri:regionArea></affiliation></author><author><name sortKey="Zhao, Yan" sort="Zhao, Yan" uniqKey="Zhao Y" first="Yan" last="Zhao">Yan Zhao</name><affiliation wicri:level="1"><nlm:aff id="au2"><institution>Biomedical Signals and Systems, MIRA Institute of Technical Medicine and Biomedical Technology, University of Twente</institution><addr-line>Enschede, The Netherlands</addr-line></nlm:aff><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Enschede</wicri:regionArea></affiliation></author><author><name sortKey="Van Gils, Stephan A" sort="Van Gils, Stephan A" uniqKey="Van Gils S" first="Stephan A" last="Van Gils">Stephan A. Van Gils</name><affiliation wicri:level="1"><nlm:aff id="au1"><institution>Applied Analysis, MIRA Institute of Technical Medicine and Biomedical Technology, University of Twente</institution><addr-line>Enschede, The Netherlands</addr-line></nlm:aff><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Enschede</wicri:regionArea></affiliation></author><author><name sortKey="Van Wezel, Richard J A" sort="Van Wezel, Richard J A" uniqKey="Van Wezel R" first="Richard J A" last="Van Wezel">Richard J A. 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Schwab</name><affiliation wicri:level="1"><nlm:aff id="au1"><institution>Applied Analysis, MIRA Institute of Technical Medicine and Biomedical Technology, University of Twente</institution><addr-line>Enschede, The Netherlands</addr-line></nlm:aff><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Enschede</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="au2"><institution>Biomedical Signals and Systems, MIRA Institute of Technical Medicine and Biomedical Technology, University of Twente</institution><addr-line>Enschede, The Netherlands</addr-line></nlm:aff><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Enschede</wicri:regionArea></affiliation></author><author><name sortKey="Heida, Tjitske" sort="Heida, Tjitske" uniqKey="Heida T" first="Tjitske" last="Heida">Tjitske Heida</name><affiliation wicri:level="1"><nlm:aff id="au2"><institution>Biomedical Signals and Systems, MIRA Institute of Technical Medicine and Biomedical Technology, University of Twente</institution><addr-line>Enschede, The Netherlands</addr-line></nlm:aff><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Enschede</wicri:regionArea></affiliation></author><author><name sortKey="Zhao, Yan" sort="Zhao, Yan" uniqKey="Zhao Y" first="Yan" last="Zhao">Yan Zhao</name><affiliation wicri:level="1"><nlm:aff id="au2"><institution>Biomedical Signals and Systems, MIRA Institute of Technical Medicine and Biomedical Technology, University of Twente</institution><addr-line>Enschede, The Netherlands</addr-line></nlm:aff><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Enschede</wicri:regionArea></affiliation></author><author><name sortKey="Van Gils, Stephan A" sort="Van Gils, Stephan A" uniqKey="Van Gils S" first="Stephan A" last="Van Gils">Stephan A. Van Gils</name><affiliation wicri:level="1"><nlm:aff id="au1"><institution>Applied Analysis, MIRA Institute of Technical Medicine and Biomedical Technology, University of Twente</institution><addr-line>Enschede, The Netherlands</addr-line></nlm:aff><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Enschede</wicri:regionArea></affiliation></author><author><name sortKey="Van Wezel, Richard J A" sort="Van Wezel, Richard J A" uniqKey="Van Wezel R" first="Richard J A" last="Van Wezel">Richard J A. Van Wezel</name><affiliation wicri:level="1"><nlm:aff id="au2"><institution>Biomedical Signals and Systems, MIRA Institute of Technical Medicine and Biomedical Technology, University of Twente</institution><addr-line>Enschede, The Netherlands</addr-line></nlm:aff><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Enschede</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="au3"><institution>Biophysics, Donders Institute for Brain, Cognition and Behavior, Radboud University</institution><addr-line>Nijmegen, The Netherlands</addr-line></nlm:aff><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Nijmegen</wicri:regionArea></affiliation></author></analytic><series><title level="j">Movement Disorders</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Basal Ganglia (metabolism)</term><term>Basal Ganglia (pathology)</term><term>Computer Simulation</term><term>Connexins (metabolism)</term><term>Female</term><term>Gap Junctions (physiology)</term><term>Globus Pallidus (metabolism)</term><term>Globus Pallidus (pathology)</term><term>Glutamate Decarboxylase (metabolism)</term><term>Humans</term><term>Male</term><term>Microscopy, Confocal</term><term>Models, Neurological</term><term>Parkinson Disease (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Connexins</term><term>Glutamate Decarboxylase</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Basal Ganglia</term><term>Globus Pallidus</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Basal Ganglia</term><term>Globus Pallidus</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Gap Junctions</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Computer Simulation</term><term>Female</term><term>Humans</term><term>Male</term><term>Microscopy, Confocal</term><term>Models, Neurological</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Although increased synchrony of the neural activity in the basal ganglia may underlie the motor deficiencies exhibited in Parkinson's disease (PD), how this synchrony arises, propagates through the basal ganglia, and changes under dopamine replacement remains unknown. Gap junctions could play a major role in modifying this synchrony, because they show functional plasticity under the influence of dopamine and after neural injury. In this study, confocal imaging was used to detect connexin-36, the major neural gap junction protein, in postmortem tissues of PD patients and control subjects in the putamen, subthalamic nucleus (STN), and external and internal globus pallidus (GPe and GPi, respectively). Moreover, we quantified how gap junctions affect synchrony in an existing computational model of the basal ganglia. We detected connexin-36 in the human putamen, GPe, and GPi, but not in the STN. Furthermore, we found that the number of connexin-36 spots in PD tissues increased by 50% in the putamen, 43% in the GPe, and 109% in the GPi compared with controls. In the computational model, gap junctions in the GPe and GPi strongly influenced synchrony. The basal ganglia became especially susceptible to synchronize with input from the cortex when gap junctions were numerous and high in conductance. In conclusion, connexin-36 expression in the human GPe and GPi suggests that gap junctional coupling exists within these nuclei. In PD, neural injury and dopamine depletion could increase this coupling. Therefore, we propose that gap junctions act as a powerful modulator of synchrony in the basal ganglia.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Wichmann, T" uniqKey="Wichmann T">T Wichmann</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Quiroga Varela, A" uniqKey="Quiroga Varela A">A Quiroga-Varela</name></author><author><name sortKey="Walters, Ja" uniqKey="Walters J">JA Walters</name></author><author><name sortKey="Brazhnik, E" uniqKey="Brazhnik E">E Brazhnik</name></author><author><name sortKey="Marin, C" uniqKey="Marin C">C Marin</name></author><author><name sortKey="Obeso, Ja" uniqKey="Obeso J">JA Obeso</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Plenz, D" uniqKey="Plenz D">D Plenz</name></author><author><name sortKey="Kital, St" uniqKey="Kital S">ST Kital</name></author></analytic></biblStruct><biblStruct><analytic><author><name 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Schwab</name></noRegion><name sortKey="Heida, Tjitske" sort="Heida, Tjitske" uniqKey="Heida T" first="Tjitske" last="Heida">Tjitske Heida</name><name sortKey="Schwab, Bettina C" sort="Schwab, Bettina C" uniqKey="Schwab B" first="Bettina C" last="Schwab">Bettina C. Schwab</name><name sortKey="Van Gils, Stephan A" sort="Van Gils, Stephan A" uniqKey="Van Gils S" first="Stephan A" last="Van Gils">Stephan A. Van Gils</name><name sortKey="Van Wezel, Richard J A" sort="Van Wezel, Richard J A" uniqKey="Van Wezel R" first="Richard J A" last="Van Wezel">Richard J A. Van Wezel</name><name sortKey="Van Wezel, Richard J A" sort="Van Wezel, Richard J A" uniqKey="Van Wezel R" first="Richard J A" last="Van Wezel">Richard J A. Van Wezel</name><name sortKey="Zhao, Yan" sort="Zhao, Yan" uniqKey="Zhao Y" first="Yan" last="Zhao">Yan Zhao</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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