Convergent evidence for abnormal striatal synaptic plasticity in dystonia
Identifieur interne : 000267 ( Ncbi/Curation ); précédent : 000266; suivant : 000268Convergent evidence for abnormal striatal synaptic plasticity in dystonia
Auteurs : David Peterson [États-Unis] ; Terrence Sejnowski [États-Unis] ; Howard Poizner [États-Unis]Source :
- Neurobiology of disease [ 0969-9961 ] ; 2009.
Abstract
Dystonia is a functionally disabling movement disorder characterized by abnormal movements and postures. Although substantial recent progress has been made in identifying genetic factors, the pathophysiology of the disease remains a mystery. A provocative suggestion gaining broader acceptance is that some aspect of neural plasticity may be abnormal. There is also evidence that, at least in some forms of dystonia, sensorimotor “use” may be a contributing factor. Most empirical evidence of abnormal plasticity in dystonia comes from measures of sensorimotor cortical organization and physiology. However, the basal ganglia also play a critical role in sensorimotor function. Furthermore, the basal ganglia are prominently implicated in traditional models of dystonia, are the primary targets of stereotactic neurosurgical interventions, and provide a neural substrate for sensorimotor learning influenced by neuromodulators. Our working hypothesis is that abnormal plasticity in the basal ganglia is a critical link between the etiology and pathophysiology of dystonia. In this review we set up the background for this hypothesis by integrating a large body of disparate indirect evidence that dystonia may involve abnormalities in synaptic plasticity in the striatum. After reviewing evidence implicating the striatum in dystonia, we focus on the influence of two neuromodulatory systems: dopamine and acetylcholine. For both of these neuromodulators, we first describe the evidence for abnormalities in dystonia and then the means by which it may influence striatal synaptic plasticity. Collectively, the evidence suggests that many different forms of dystonia may involve abnormal plasticity in the striatum. An improved understanding of these altered plastic processes would help inform our understanding of the pathophysiology of dystonia, and, given the role of the striatum in sensorimotor learning, provide a principled basis for designing therapies aimed at the dynamic processes linking etiology to pathophysiology of the disease.
Url:
DOI: 10.1016/j.nbd.2009.12.003
PubMed: 20005952
PubMed Central: 2846420
Links toward previous steps (curation, corpus...)
- to stream Pmc, to step Corpus: Pour aller vers cette notice dans l'étape Curation :000202
- to stream Pmc, to step Curation: Pour aller vers cette notice dans l'étape Curation :000202
- to stream Pmc, to step Checkpoint: Pour aller vers cette notice dans l'étape Curation :000200
- to stream Ncbi, to step Merge: Pour aller vers cette notice dans l'étape Curation :000267
Links to Exploration step
PMC:2846420Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Convergent evidence for abnormal striatal synaptic plasticity in dystonia</title>
<author><name sortKey="Peterson, David A" sort="Peterson, David A" uniqKey="Peterson D" first="David" last="Peterson">David Peterson</name>
<affiliation wicri:level="2"><nlm:aff id="A1">Institute for Neural Computation, University of California at San Diego, La Jolla, CA 92093, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Institute for Neural Computation, University of California at San Diego, La Jolla, CA 92093</wicri:regionArea>
<placeName><region type="state">Californie</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Sejnowski, Terrence J" sort="Sejnowski, Terrence J" uniqKey="Sejnowski T" first="Terrence" last="Sejnowski">Terrence Sejnowski</name>
<affiliation wicri:level="2"><nlm:aff id="A1">Institute for Neural Computation, University of California at San Diego, La Jolla, CA 92093, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Institute for Neural Computation, University of California at San Diego, La Jolla, CA 92093</wicri:regionArea>
<placeName><region type="state">Californie</region>
</placeName>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="A2">Howard Hughes Medical Institute, Computational Neurobiology Laboratory, The Salk Institute for Biological Studies, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Howard Hughes Medical Institute, Computational Neurobiology Laboratory, The Salk Institute for Biological Studies</wicri:regionArea>
<wicri:noRegion>The Salk Institute for Biological Studies</wicri:noRegion>
</affiliation>
<affiliation wicri:level="2"><nlm:aff id="A3">Division of Biological Sciences, University of California at San Diego, La Jolla, CA 92093, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Division of Biological Sciences, University of California at San Diego, La Jolla, CA 92093</wicri:regionArea>
<placeName><region type="state">Californie</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Poizner, Howard" sort="Poizner, Howard" uniqKey="Poizner H" first="Howard" last="Poizner">Howard Poizner</name>
<affiliation wicri:level="2"><nlm:aff id="A1">Institute for Neural Computation, University of California at San Diego, La Jolla, CA 92093, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Institute for Neural Computation, University of California at San Diego, La Jolla, CA 92093</wicri:regionArea>
<placeName><region type="state">Californie</region>
</placeName>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">20005952</idno>
<idno type="pmc">2846420</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2846420</idno>
<idno type="RBID">PMC:2846420</idno>
<idno type="doi">10.1016/j.nbd.2009.12.003</idno>
<date when="2009">2009</date>
<idno type="wicri:Area/Pmc/Corpus">000202</idno>
<idno type="wicri:Area/Pmc/Curation">000202</idno>
<idno type="wicri:Area/Pmc/Checkpoint">000200</idno>
<idno type="wicri:Area/Ncbi/Merge">000267</idno>
<idno type="wicri:Area/Ncbi/Curation">000267</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Convergent evidence for abnormal striatal synaptic plasticity in dystonia</title>
<author><name sortKey="Peterson, David A" sort="Peterson, David A" uniqKey="Peterson D" first="David" last="Peterson">David Peterson</name>
<affiliation wicri:level="2"><nlm:aff id="A1">Institute for Neural Computation, University of California at San Diego, La Jolla, CA 92093, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Institute for Neural Computation, University of California at San Diego, La Jolla, CA 92093</wicri:regionArea>
<placeName><region type="state">Californie</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Sejnowski, Terrence J" sort="Sejnowski, Terrence J" uniqKey="Sejnowski T" first="Terrence" last="Sejnowski">Terrence Sejnowski</name>
<affiliation wicri:level="2"><nlm:aff id="A1">Institute for Neural Computation, University of California at San Diego, La Jolla, CA 92093, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Institute for Neural Computation, University of California at San Diego, La Jolla, CA 92093</wicri:regionArea>
<placeName><region type="state">Californie</region>
</placeName>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="A2">Howard Hughes Medical Institute, Computational Neurobiology Laboratory, The Salk Institute for Biological Studies, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Howard Hughes Medical Institute, Computational Neurobiology Laboratory, The Salk Institute for Biological Studies</wicri:regionArea>
<wicri:noRegion>The Salk Institute for Biological Studies</wicri:noRegion>
</affiliation>
<affiliation wicri:level="2"><nlm:aff id="A3">Division of Biological Sciences, University of California at San Diego, La Jolla, CA 92093, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Division of Biological Sciences, University of California at San Diego, La Jolla, CA 92093</wicri:regionArea>
<placeName><region type="state">Californie</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Poizner, Howard" sort="Poizner, Howard" uniqKey="Poizner H" first="Howard" last="Poizner">Howard Poizner</name>
<affiliation wicri:level="2"><nlm:aff id="A1">Institute for Neural Computation, University of California at San Diego, La Jolla, CA 92093, USA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Institute for Neural Computation, University of California at San Diego, La Jolla, CA 92093</wicri:regionArea>
<placeName><region type="state">Californie</region>
</placeName>
</affiliation>
</author>
</analytic>
<series><title level="j">Neurobiology of disease</title>
<idno type="ISSN">0969-9961</idno>
<idno type="e-ISSN">1095-953X</idno>
<imprint><date when="2009">2009</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p id="P1">Dystonia is a functionally disabling movement disorder characterized by abnormal movements and postures. Although substantial recent progress has been made in identifying genetic factors, the pathophysiology of the disease remains a mystery. A provocative suggestion gaining broader acceptance is that some aspect of neural plasticity may be abnormal. There is also evidence that, at least in some forms of dystonia, sensorimotor “use” may be a contributing factor. Most empirical evidence of abnormal plasticity in dystonia comes from measures of sensorimotor cortical organization and physiology. However, the basal ganglia also play a critical role in sensorimotor function. Furthermore, the basal ganglia are prominently implicated in traditional models of dystonia, are the primary targets of stereotactic neurosurgical interventions, and provide a neural substrate for sensorimotor learning influenced by neuromodulators. Our working hypothesis is that abnormal plasticity in the basal ganglia is a critical link between the etiology and pathophysiology of dystonia. In this review we set up the background for this hypothesis by integrating a large body of disparate indirect evidence that dystonia may involve abnormalities in synaptic plasticity in the striatum. After reviewing evidence implicating the striatum in dystonia, we focus on the influence of two neuromodulatory systems: dopamine and acetylcholine. For both of these neuromodulators, we first describe the evidence for abnormalities in dystonia and then the means by which it may influence striatal synaptic plasticity. Collectively, the evidence suggests that many different forms of dystonia may involve abnormal plasticity in the striatum. An improved understanding of these altered plastic processes would help inform our understanding of the pathophysiology of dystonia, and, given the role of the striatum in sensorimotor learning, provide a principled basis for designing therapies aimed at the dynamic processes linking etiology to pathophysiology of the disease.</p>
</div>
</front>
</TEI>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/JankovicV1/Data/Ncbi/Curation
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000267 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Ncbi/Curation/biblio.hfd -nk 000267 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Santé |area= JankovicV1 |flux= Ncbi |étape= Curation |type= RBID |clé= PMC:2846420 |texte= Convergent evidence for abnormal striatal synaptic plasticity in dystonia }}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Ncbi/Curation/RBID.i -Sk "pubmed:20005952" \ | HfdSelect -Kh $EXPLOR_AREA/Data/Ncbi/Curation/biblio.hfd \ | NlmPubMed2Wicri -a JankovicV1
![]() | This area was generated with Dilib version V0.6.19. | ![]() |