Balancing the basal ganglia circuitry: a possible new role for dopamine D2 receptors in health and disease.
Identifieur interne : 000314 ( PubMed/Checkpoint ); précédent : 000313; suivant : 000315Balancing the basal ganglia circuitry: a possible new role for dopamine D2 receptors in health and disease.
Auteurs : Maxime Cazorla [États-Unis] ; Un Jung Kang [États-Unis] ; Christoph Kellendonk [États-Unis]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2015.
Abstract
Current therapies for treating movement disorders such as Parkinson's disease are effective but limited by undesirable and intractable side effects. Developing more effective therapies will require better understanding of what causes basal ganglia dysregulation and why medication-induced side effects develop. Although basal ganglia have been extensively studied in the last decades, its circuit anatomy is very complex, and significant controversy exists as to how the interplay of different basal ganglia nuclei process motor information and output. We have recently identified the importance of an underappreciated collateral projection that bridges the striatal output direct pathway with the indirect pathway. These bridging collaterals are extremely plastic in the adult brain and are involved in the regulation of motor balance. Our findings add a new angle to the classical model of basal ganglia circuitry that could be exploited for the development of new therapies against movement disorders. In this Scientific Perspective, we describe the function of bridging collaterals and other recent discoveries that challenge the simplicity of the classical basal ganglia circuit model. We then discuss the potential implication of bridging collaterals in the pathophysiology of Parkinson's disease and schizophrenia. Because dopamine D2 receptors and striatal neuron excitability have been found to regulate the density of bridging collaterals, we propose that targeting these projections downstream of D2 receptors could be a possible strategy for the treatment of basal ganglia disorders. © 2015 International Parkinson and Movement Disorder Society.
DOI: 10.1002/mds.26282
PubMed: 26018615
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Developing more effective therapies will require better understanding of what causes basal ganglia dysregulation and why medication-induced side effects develop. Although basal ganglia have been extensively studied in the last decades, its circuit anatomy is very complex, and significant controversy exists as to how the interplay of different basal ganglia nuclei process motor information and output. We have recently identified the importance of an underappreciated collateral projection that bridges the striatal output direct pathway with the indirect pathway. These bridging collaterals are extremely plastic in the adult brain and are involved in the regulation of motor balance. Our findings add a new angle to the classical model of basal ganglia circuitry that could be exploited for the development of new therapies against movement disorders. In this Scientific Perspective, we describe the function of bridging collaterals and other recent discoveries that challenge the simplicity of the classical basal ganglia circuit model. We then discuss the potential implication of bridging collaterals in the pathophysiology of Parkinson's disease and schizophrenia. Because dopamine D2 receptors and striatal neuron excitability have been found to regulate the density of bridging collaterals, we propose that targeting these projections downstream of D2 receptors could be a possible strategy for the treatment of basal ganglia disorders. © 2015 International Parkinson and Movement Disorder Society.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="In-Process"><PMID Version="1">26018615</PMID><DateCreated><Year>2015</Year><Month>06</Month><Day>23</Day></DateCreated><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>30</Volume><Issue>7</Issue><PubDate><Year>2015</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. 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We have recently identified the importance of an underappreciated collateral projection that bridges the striatal output direct pathway with the indirect pathway. These bridging collaterals are extremely plastic in the adult brain and are involved in the regulation of motor balance. Our findings add a new angle to the classical model of basal ganglia circuitry that could be exploited for the development of new therapies against movement disorders. In this Scientific Perspective, we describe the function of bridging collaterals and other recent discoveries that challenge the simplicity of the classical basal ganglia circuit model. We then discuss the potential implication of bridging collaterals in the pathophysiology of Parkinson's disease and schizophrenia. Because dopamine D2 receptors and striatal neuron excitability have been found to regulate the density of bridging collaterals, we propose that targeting these projections downstream of D2 receptors could be a possible strategy for the treatment of basal ganglia disorders. © 2015 International Parkinson and Movement Disorder Society.</AbstractText><CopyrightInformation>© 2015 International Parkinson and Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Cazorla</LastName><ForeName>Maxime</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Psychiatry, Columbia University, New York, New York, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pharmacology, Columbia University, New York, New York, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Molecular Therapeutics, New York State Psychiatric Institute, New York, New York, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kang</LastName><ForeName>Un Jung</ForeName><Initials>UJ</Initials><AffiliationInfo><Affiliation>Department of Neurology, Columbia University, New York, New York, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kellendonk</LastName><ForeName>Christoph</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Psychiatry, Columbia University, New York, New York, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pharmacology, Columbia University, New York, New York, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Molecular Therapeutics, New York State Psychiatric Institute, New York, New York, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>MH086404</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01MH093672</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01NS064439</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>05</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Dopamine receptors</Keyword><Keyword MajorTopicYN="N">Parkinson's disease</Keyword><Keyword MajorTopicYN="N">bridging collaterals</Keyword><Keyword MajorTopicYN="N">direct and indirect pathways</Keyword><Keyword MajorTopicYN="N">dyskinesia</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>1</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2015</Year><Month>5</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>5</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="aheadofprint"><Year>2015</Year><Month>5</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>5</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>5</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>5</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26018615</ArticleId><ArticleId IdType="doi">10.1002/mds.26282</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>État de New York</li></region><settlement><li>New York</li></settlement><orgName><li>Université Columbia</li></orgName></list><tree><country name="États-Unis"><region name="État de New York"><name sortKey="Cazorla, Maxime" sort="Cazorla, Maxime" uniqKey="Cazorla M" first="Maxime" last="Cazorla">Maxime Cazorla</name></region><name sortKey="Kang, Un Jung" sort="Kang, Un Jung" uniqKey="Kang U" first="Un Jung" last="Kang">Un Jung Kang</name><name sortKey="Kellendonk, Christoph" sort="Kellendonk, Christoph" uniqKey="Kellendonk C" first="Christoph" last="Kellendonk">Christoph Kellendonk</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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