ParkinsonCanadaV1, Pmc, Curation, bibRecord, 000881

Selective loss of bi-directional synaptic plasticity in the direct and indirect striatal output pathways accompanies generation of parkinsonism and l-DOPA induced dyskinesia in mouse models

Identifieur interne : 000881 ( Pmc/Curation ); précédent : 000880; suivant : 000882

Selective loss of bi-directional synaptic plasticity in the direct and indirect striatal output pathways accompanies generation of parkinsonism and l-DOPA induced dyskinesia in mouse models

Auteurs : Sherri L. Thiele [Canada] ; Betty Chen [Canada] ; Charlotte Lo [Canada] ; Tracey S. Gertler [États-Unis] ; Ruth Warre [Canada] ; James D. Surmeier [États-Unis] ; Jonathan M. Brotchie [Canada] ; Joanne E. Nash [Canada]

Source :

Neurobiology of disease [ 0969-9961 ] ; 2014.

RBID : PMC:4486078

Abstract

Parkinsonian symptoms arise due to over-activity of the indirect striatal output pathway, and under-activity of the direct striatal output pathway. l-DOPA-induced dyskinesia (LID) is caused when the opposite circuitry problems are established, with the indirect pathway becoming underactive, and the direct pathway becoming over-active. Here, we define synaptic plasticity abnormalities in these pathways associated with parkinsonism, symptomatic benefits of l-DOPA, and LID. We applied spike-timing dependent plasticity protocols to corticostriatal synapses in slices from 6-OHDA-lesioned mouse models of parkinsonism and LID, generated in BAC transgenic mice with eGFP targeting the direct or indirect output pathways, with and without l-DOPA present. In naïve mice, bidirectional synaptic plasticity, i.e. LTP and LTD, was induced, resulting in an EPSP amplitude change of approximately 50% in each direction in both striatal output pathways, as shown previously. In parkinsonism and dyskinesia, both pathways exhibited unidirectional plasticity, irrespective of stimulation paradigm. In parkinsonian animals, the indirect pathway only exhibited LTP (LTP protocol: 143.5 ± 14.6%; LTD protocol 177.7 ± 22.3% of baseline), whereas the direct pathway only showed LTD (LTP protocol: 74.3 ± 4.0% and LTD protocol: 63.3 ± 8.7%). A symptomatic dose of l-DOPA restored bidirectional plasticity on both pathways to levels comparable to naïve animals (Indirect pathway: LTP protocol: 124.4± 22.0% and LTD protocol: 52.1± 18.5% of baseline. Direct pathway: LTP protocol: 140.7 ± 7.3% and LTD protocol: 58.4 ± 6.0% of baseline). In dyskinesia, in the presence of l-DOPA, the indirect pathway exhibited only LTD (LTP protocol: 68.9 ± 21.3% and LTD protocol 52.0 ± 14.2% of baseline), whereas in the direct pathway, only LTP could be induced (LTP protocol: 156.6 ± 13.2% and LTD protocol 166.7 ± 15.8% of baseline). We conclude that normal motor control requires bidirectional plasticity of both striatal outputs, which underlies the symptomatic benefits of l-DOPA. Switching from bidirectional to unidirectional plasticity drives global changes in striatal pathway excitability, and underpins parkinsonism and dyskinesia.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4486078

DOI: 10.1016/j.nbd.2014.08.006
PubMed: 25171793
PubMed Central: 4486078

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-DOPA induced dyskinesia in mouse models</title>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Selective loss of bi-directional synaptic plasticity in the direct and indirect striatal output pathways accompanies generation of parkinsonism and <sc>l</sc>
-DOPA induced dyskinesia in mouse models</title>
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<wicri:regionArea>Division of Brain Imaging & Behaviour Systems — Neuroscience, Toronto Western Research Institute, 399 Bathurst Street, Toronto, ON M5T 2S8</wicri:regionArea>
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<author><name sortKey="Nash, Joanne E" sort="Nash, Joanne E" uniqKey="Nash J" first="Joanne E." last="Nash">Joanne E. Nash</name>
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<series><title level="j">Neurobiology of disease</title>
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<front><div type="abstract" xml:lang="en"><p id="P1">Parkinsonian symptoms arise due to over-activity of the indirect striatal output pathway, and under-activity of the direct striatal output pathway. <sc>l</sc>
-DOPA-induced dyskinesia (LID) is caused when the opposite circuitry problems are established, with the indirect pathway becoming underactive, and the direct pathway becoming over-active. Here, we define synaptic plasticity abnormalities in these pathways associated with parkinsonism, symptomatic benefits of <sc>l</sc>
-DOPA, and LID. We applied spike-timing dependent plasticity protocols to corticostriatal synapses in slices from 6-OHDA-lesioned mouse models of parkinsonism and LID, generated in BAC transgenic mice with eGFP targeting the direct or indirect output pathways, with and without <sc>l</sc>
-DOPA present. In naïve mice, bidirectional synaptic plasticity, i.e. LTP and LTD, was induced, resulting in an EPSP amplitude change of approximately 50% in each direction in both striatal output pathways, as shown previously. In parkinsonism and dyskinesia, both pathways exhibited unidirectional plasticity, irrespective of stimulation paradigm. In parkinsonian animals, the indirect pathway only exhibited LTP (LTP protocol: 143.5 ± 14.6%; LTD protocol 177.7 ± 22.3% of baseline), whereas the direct pathway only showed LTD (LTP protocol: 74.3 ± 4.0% and LTD protocol: 63.3 ± 8.7%). A symptomatic dose of <sc>l</sc>
-DOPA restored bidirectional plasticity on both pathways to levels comparable to naïve animals (Indirect pathway: LTP protocol: 124.4± 22.0% and LTD protocol: 52.1± 18.5% of baseline. Direct pathway: LTP protocol: 140.7 ± 7.3% and LTD protocol: 58.4 ± 6.0% of baseline). In dyskinesia, in the presence of <sc>l</sc>
-DOPA, the indirect pathway exhibited only LTD (LTP protocol: 68.9 ± 21.3% and LTD protocol 52.0 ± 14.2% of baseline), whereas in the direct pathway, only LTP could be induced (LTP protocol: 156.6 ± 13.2% and LTD protocol 166.7 ± 15.8% of baseline). We conclude that normal motor control requires bidirectional plasticity of both striatal outputs, which underlies the symptomatic benefits of <sc>l</sc>
-DOPA. Switching from bidirectional to unidirectional plasticity drives global changes in striatal pathway excitability, and underpins parkinsonism and dyskinesia.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
  <pmc-dir>properties manuscript</pmc-dir>
  <front><journal-meta><journal-id journal-id-type="nlm-journal-id">9500169</journal-id>
<journal-id journal-id-type="pubmed-jr-id">20475</journal-id>
<journal-id journal-id-type="nlm-ta">Neurobiol Dis</journal-id>
<journal-id journal-id-type="iso-abbrev">Neurobiol. Dis.</journal-id>
<journal-title-group><journal-title>Neurobiology of disease</journal-title>
</journal-title-group>
<issn pub-type="ppub">0969-9961</issn>
<issn pub-type="epub">1095-953X</issn>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">25171793</article-id>
<article-id pub-id-type="pmc">4486078</article-id>
<article-id pub-id-type="doi">10.1016/j.nbd.2014.08.006</article-id>
<article-id pub-id-type="manuscript">NIHMS687314</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Selective loss of bi-directional synaptic plasticity in the direct and indirect striatal output pathways accompanies generation of parkinsonism and <sc>l</sc>
-DOPA induced dyskinesia in mouse models</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Thiele</surname>
<given-names>Sherri L.</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Chen</surname>
<given-names>Betty</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Lo</surname>
<given-names>Charlotte</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Gertler</surname>
<given-names>Tracey S.</given-names>
</name>
<xref ref-type="aff" rid="A3">c</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Warre</surname>
<given-names>Ruth</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Surmeier</surname>
<given-names>James D.</given-names>
</name>
<xref ref-type="aff" rid="A3">c</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Brotchie</surname>
<given-names>Jonathan M.</given-names>
</name>
<xref ref-type="aff" rid="A2">b</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Nash</surname>
<given-names>Joanne E.</given-names>
</name>
<xref ref-type="aff" rid="A1">a</xref>
<xref ref-type="corresp" rid="cor1">*</xref>
</contrib>
</contrib-group>
<aff id="A1"><label>a</label>
Centre for Neurobiology of Stress, Department of Biological Sciences, University of Toronto Scarborough, 1265 Military Trail, Toronto, ON M1C 1A4, Canada</aff>
<aff id="A2"><label>b</label>
Division of Brain Imaging & Behaviour Systems — Neuroscience, Toronto Western Research Institute, 399 Bathurst Street, Toronto, ON M5T 2S8, Canada</aff>
<aff id="A3"><label>c</label>
Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA</aff>
<author-notes><corresp id="cor1"><label>*</label>
Corresponding author. Fax: +1 416 287 7676. <email>jnash@utsc.utoronto.ca</email>
 (J.E. Nash)</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>6</day>
<month>5</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="epub"><day>27</day>
<month>8</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="ppub"><month>11</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>30</day>
<month>6</month>
<year>2015</year>
</pub-date>
<volume>71</volume>
<fpage>334</fpage>
<lpage>344</lpage>
<pmc-comment>elocation-id from pubmed: 10.1016/j.nbd.2014.08.006</pmc-comment>
      <permissions><copyright-statement>Copyright © 2014 Published by Elsevier Inc. All rights reserved.</copyright-statement>
<copyright-year>2014</copyright-year>
</permissions>
<abstract><p id="P1">Parkinsonian symptoms arise due to over-activity of the indirect striatal output pathway, and under-activity of the direct striatal output pathway. <sc>l</sc>
-DOPA-induced dyskinesia (LID) is caused when the opposite circuitry problems are established, with the indirect pathway becoming underactive, and the direct pathway becoming over-active. Here, we define synaptic plasticity abnormalities in these pathways associated with parkinsonism, symptomatic benefits of <sc>l</sc>
-DOPA, and LID. We applied spike-timing dependent plasticity protocols to corticostriatal synapses in slices from 6-OHDA-lesioned mouse models of parkinsonism and LID, generated in BAC transgenic mice with eGFP targeting the direct or indirect output pathways, with and without <sc>l</sc>
-DOPA present. In naïve mice, bidirectional synaptic plasticity, i.e. LTP and LTD, was induced, resulting in an EPSP amplitude change of approximately 50% in each direction in both striatal output pathways, as shown previously. In parkinsonism and dyskinesia, both pathways exhibited unidirectional plasticity, irrespective of stimulation paradigm. In parkinsonian animals, the indirect pathway only exhibited LTP (LTP protocol: 143.5 ± 14.6%; LTD protocol 177.7 ± 22.3% of baseline), whereas the direct pathway only showed LTD (LTP protocol: 74.3 ± 4.0% and LTD protocol: 63.3 ± 8.7%). A symptomatic dose of <sc>l</sc>
-DOPA restored bidirectional plasticity on both pathways to levels comparable to naïve animals (Indirect pathway: LTP protocol: 124.4± 22.0% and LTD protocol: 52.1± 18.5% of baseline. Direct pathway: LTP protocol: 140.7 ± 7.3% and LTD protocol: 58.4 ± 6.0% of baseline). In dyskinesia, in the presence of <sc>l</sc>
-DOPA, the indirect pathway exhibited only LTD (LTP protocol: 68.9 ± 21.3% and LTD protocol 52.0 ± 14.2% of baseline), whereas in the direct pathway, only LTP could be induced (LTP protocol: 156.6 ± 13.2% and LTD protocol 166.7 ± 15.8% of baseline). We conclude that normal motor control requires bidirectional plasticity of both striatal outputs, which underlies the symptomatic benefits of <sc>l</sc>
-DOPA. Switching from bidirectional to unidirectional plasticity drives global changes in striatal pathway excitability, and underpins parkinsonism and dyskinesia.</p>
</abstract>
<kwd-group><kwd>Parkinson’s disease</kwd>
<kwd>Dyskinesia</kwd>
<kwd>BAC transgenic mouse models</kwd>
<kwd>Slice electrophysiology</kwd>
<kwd>Striatum</kwd>
<kwd>Synaptic plasticity</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>

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	La maladie de Parkinson au Canada (serveur d'exploration)
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Selective loss of bi-directional synaptic plasticity in the direct and indirect striatal output pathways accompanies generation of parkinsonism and l-DOPA induced dyskinesia in mouse models

Selective loss of bi-directional synaptic plasticity in the direct and indirect striatal output pathways accompanies generation of parkinsonism and l-DOPA induced dyskinesia in mouse models

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Abstract

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