ParkinsonFranceV1, Hal, Corpus, bibRecord, 000331

Dopamine-dependent long-term depression at subthalamo-nigral synapses is lost in experimental parkinsonism.

Identifieur interne : 000331 ( Hal/Corpus ); précédent : 000330; suivant : 000332

Dopamine-dependent long-term depression at subthalamo-nigral synapses is lost in experimental parkinsonism.

Auteurs : Julien Pierre Dupuis ; Michael Feyder ; Cristina Miguelez ; Liliana Garcia ; Stéphanie Morin ; Daniel Choquet ; Eric Hosy ; Erwan Bezard ; Gilberto Fisone ; Bernard H. Bioulac ; Jérôme Baufreton

Source :

Journal of Neuroscience [ 0270-6474 ] ; 2013-09-04.

RBID : Hal:hal-01155166

Abstract

Impairments of synaptic plasticity are a hallmark of several neurological disorders, including Parkinson's disease (PD) which results from the progressive loss of dopaminergic neurons of the substantia nigra pars compacta leading to abnormal activity within the basal ganglia (BG) network and pathological motor symptoms. Indeed, disrupted plasticity at corticostriatal glutamatergic synapses, the gateway of the BG, is correlated to the onset of PD-related movement disorders and thus has been proposed to be a key neural substrate regulating information flow and motor function in BG circuits. However, a critical question is whether similar plasticity impairments could occur at other glutamatergic connections within the BG that would also affect the inhibitory influence of the network on the motor thalamus. Here, we show that long-term plasticity at subthalamo-nigral glutamatergic synapses (STN-SNr) sculpting the activity patterns of nigral neurons, the main output of the network, is also affected in experimental parkinsonism. Using whole-cell patch-clamp in acute rat brain slices, we describe a molecular pathway supporting an activity-dependent long-term depression of STN-SNr synapses through an NMDAR-and D1/5 dopamine receptor-mediated endocytosis of synaptic AMPA glutamate receptors. We also show that this plastic property is lost in an experimental rat model of PD but can be restored through the recruitment of dopamine D1/5 receptors. Altogether, our findings suggest that pathological impairments of subthalamo-nigral plasticity may enhance BG outputs and thereby contribute to PD-related motor dysfunctions.

Url:

https://hal.archives-ouvertes.fr/hal-01155166

DOI: 10.1523/JNEUROSCI.1681-13.2013

Links to Exploration step

Hal:hal-01155166

Le document en format XML

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<idno type="DOI">10.1523/JNEUROSCI.1681-13.2013</idno>
<series><title level="j">Journal of Neuroscience</title>
<idno type="ISSN">0270-6474</idno>
<imprint><date type="datePub">2013-09-04</date>
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<front><div type="abstract" xml:lang="en">Impairments of synaptic plasticity are a hallmark of several neurological disorders, including Parkinson's disease (PD) which results from the progressive loss of dopaminergic neurons of the substantia nigra pars compacta leading to abnormal activity within the basal ganglia (BG) network and pathological motor symptoms. Indeed, disrupted plasticity at corticostriatal glutamatergic synapses, the gateway of the BG, is correlated to the onset of PD-related movement disorders and thus has been proposed to be a key neural substrate regulating information flow and motor function in BG circuits. However, a critical question is whether similar plasticity impairments could occur at other glutamatergic connections within the BG that would also affect the inhibitory influence of the network on the motor thalamus. Here, we show that long-term plasticity at subthalamo-nigral glutamatergic synapses (STN-SNr) sculpting the activity patterns of nigral neurons, the main output of the network, is also affected in experimental parkinsonism. Using whole-cell patch-clamp in acute rat brain slices, we describe a molecular pathway supporting an activity-dependent long-term depression of STN-SNr synapses through an NMDAR-and D1/5 dopamine receptor-mediated endocytosis of synaptic AMPA glutamate receptors. We also show that this plastic property is lost in an experimental rat model of PD but can be restored through the recruitment of dopamine D1/5 receptors. Altogether, our findings suggest that pathological impairments of subthalamo-nigral plasticity may enhance BG outputs and thereby contribute to PD-related motor dysfunctions.</div>
</front>
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<hal api="V3"><titleStmt><title xml:lang="en">Dopamine-dependent long-term depression at subthalamo-nigral synapses is lost in experimental parkinsonism.</title>
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<surname>Dupuis</surname>
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<author role="aut"><persName><forename type="first">Michael</forename>
<surname>Feyder</surname>
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<idno type="halauthorid">1169179</idno>
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<author role="aut"><persName><forename type="first">Cristina</forename>
<surname>Miguelez</surname>
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<idno type="halauthorid">1169180</idno>
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<author role="aut"><persName><forename type="first">Liliana</forename>
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<editionStmt><edition n="v1" type="current"><date type="whenSubmitted">2015-05-26 11:37:35</date>
<date type="whenModified">2015-05-27 01:00:19</date>
<date type="whenReleased">2015-05-26 11:37:35</date>
<date type="whenProduced">2013-09-04</date>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Dopamine-dependent long-term depression at subthalamo-nigral synapses is lost in experimental parkinsonism.</title>
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<author role="aut"><persName><forename type="first">Cristina</forename>
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<author role="aut"><persName><forename type="first">Liliana</forename>
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<affiliation ref="#struct-244085"></affiliation>
</author>
<author role="aut"><persName><forename type="first">Stéphanie</forename>
<surname>Morin</surname>
</persName>
<idno type="halauthorid">804107</idno>
<affiliation ref="#struct-244085"></affiliation>
</author>
<author role="aut"><persName><forename type="first">Daniel</forename>
<surname>Choquet</surname>
</persName>
<idno type="halauthorid">61647</idno>
<affiliation ref="#struct-229971"></affiliation>
</author>
<author role="aut"><persName><forename type="first">Eric</forename>
<surname>Hosy</surname>
</persName>
<idno type="halauthorid">241671</idno>
<affiliation ref="#struct-229971"></affiliation>
</author>
<author role="aut"><persName><forename type="first">Erwan</forename>
<surname>Bezard</surname>
</persName>
<idno type="halauthorid">537314</idno>
<affiliation ref="#struct-244085"></affiliation>
</author>
<author role="aut"><persName><forename type="first">Gilberto</forename>
<surname>Fisone</surname>
</persName>
<idno type="halauthorid">224336</idno>
<affiliation ref="#struct-262808"></affiliation>
</author>
<author role="aut"><persName><forename type="first">Bernard H</forename>
<surname>Bioulac</surname>
</persName>
<idno type="halauthorid">1169075</idno>
<affiliation ref="#struct-244085"></affiliation>
</author>
<author role="aut"><persName><forename type="first">Jérôme</forename>
<surname>Baufreton</surname>
</persName>
<idno type="halauthorid">1061388</idno>
<affiliation ref="#struct-244085"></affiliation>
</author>
</analytic>
<monogr><idno type="halJournalId" status="VALID">6330</idno>
<idno type="issn">0270-6474</idno>
<idno type="eissn">1529-2401</idno>
<title level="j">Journal of Neuroscience</title>
<imprint><publisher>Society for Neuroscience</publisher>
<biblScope unit="volume">33</biblScope>
<biblScope unit="issue">36</biblScope>
<biblScope unit="pp">14331-41</biblScope>
<date type="datePub">2013-09-04</date>
</imprint>
</monogr>
<idno type="pubmed">24005286</idno>
<idno type="doi">10.1523/JNEUROSCI.1681-13.2013</idno>
</biblStruct>
</sourceDesc>
<profileDesc><langUsage><language ident="en">English</language>
</langUsage>
<textClass><classCode scheme="mesh">Animals</classCode>
<classCode scheme="mesh">Dopamine</classCode>
<classCode scheme="mesh">Receptors, Dopamine D5</classCode>
<classCode scheme="mesh">Receptors, N-Methyl-D-Aspartate</classCode>
<classCode scheme="mesh">Substantia Nigra</classCode>
<classCode scheme="mesh">Synapses</classCode>
<classCode scheme="mesh">Thalamus</classCode>
<classCode scheme="mesh">Dopaminergic Neurons</classCode>
<classCode scheme="mesh">Endocytosis</classCode>
<classCode scheme="mesh">Long-Term Synaptic Depression</classCode>
<classCode scheme="mesh">Male</classCode>
<classCode scheme="mesh">Parkinsonian Disorders</classCode>
<classCode scheme="mesh">Rats</classCode>
<classCode scheme="mesh">Rats, Sprague-Dawley</classCode>
<classCode scheme="mesh">Receptors, AMPA</classCode>
<classCode scheme="halDomain" n="sdv.neu.nb">Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology</classCode>
<classCode scheme="halTypology" n="ART">Journal articles</classCode>
</textClass>
<abstract xml:lang="en">Impairments of synaptic plasticity are a hallmark of several neurological disorders, including Parkinson's disease (PD) which results from the progressive loss of dopaminergic neurons of the substantia nigra pars compacta leading to abnormal activity within the basal ganglia (BG) network and pathological motor symptoms. Indeed, disrupted plasticity at corticostriatal glutamatergic synapses, the gateway of the BG, is correlated to the onset of PD-related movement disorders and thus has been proposed to be a key neural substrate regulating information flow and motor function in BG circuits. However, a critical question is whether similar plasticity impairments could occur at other glutamatergic connections within the BG that would also affect the inhibitory influence of the network on the motor thalamus. Here, we show that long-term plasticity at subthalamo-nigral glutamatergic synapses (STN-SNr) sculpting the activity patterns of nigral neurons, the main output of the network, is also affected in experimental parkinsonism. Using whole-cell patch-clamp in acute rat brain slices, we describe a molecular pathway supporting an activity-dependent long-term depression of STN-SNr synapses through an NMDAR-and D1/5 dopamine receptor-mediated endocytosis of synaptic AMPA glutamate receptors. We also show that this plastic property is lost in an experimental rat model of PD but can be restored through the recruitment of dopamine D1/5 receptors. Altogether, our findings suggest that pathological impairments of subthalamo-nigral plasticity may enhance BG outputs and thereby contribute to PD-related motor dysfunctions.</abstract>
</profileDesc>
</hal>
</record>

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	La maladie de Parkinson en France (serveur d'exploration)
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La maladie de Parkinson en France (serveur d'exploration)

Dopamine-dependent long-term depression at subthalamo-nigral synapses is lost in experimental parkinsonism.

Dopamine-dependent long-term depression at subthalamo-nigral synapses is lost in experimental parkinsonism.

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