INTRAPALLIDAL ADMINISTRATION OF 6-HYDROXYDOPAMINE MIMICS IN LARGE PART THE ELECTROPHYSIOLOGICAL AND BEHAVIORAL CONSEQUENCES OF MAJOR DOPAMINE DEPLETION IN THE RAT
Identifieur interne : 000114 ( PascalFrancis/Corpus ); précédent : 000113; suivant : 000115INTRAPALLIDAL ADMINISTRATION OF 6-HYDROXYDOPAMINE MIMICS IN LARGE PART THE ELECTROPHYSIOLOGICAL AND BEHAVIORAL CONSEQUENCES OF MAJOR DOPAMINE DEPLETION IN THE RAT
Auteurs : P. M. Abedi ; C. Delaville ; P. De Deurwaerdere ; W. Benjelloun ; A. BenazzouzSource :
- Neuroscience [ 0306-4522 ] ; 2013.
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- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
In addition to GABA and glutamate innervations, the globus pallidus (GP) receives dopamine afferents from the pars compacta of the substantia nigra (SNc), and in turn, sends inhibitory GABAergic efferents to the subthalamic nucleus (STN) and the pars reticulata of the substantia nigra (SNr). Nevertheless, the role of dopamine in the modulation of these pallido-subthalamic and pallido-nigral projections is not known. The present study aimed to investigate the effects of intrapallidal injection of 6-hydroxydopamine (6-OHDA) on the electrical activity of STN and SNr neurons using in vivo extracellular single unit recordings in the rat and on motor behaviors, using the "open field" actimeter and the stepping test. We show that intrapallidal injection of 6-OHDA significantly decreased locomotor activity and contralateral paw use. Electrophysiological recordings show that 6-OHDA injection into GP significantly increased the number of bursty cells in the STN without changing the firing rate, while in the SNr neuronal firing rate decreased and the proportion of irregular cells increased. Our data provide evidence that intrapallidal injection of 6-OHDA resulted in motor deficits paralleled by changes in the firing activity of STN and SNr neurons, which mimic in large part those obtained after major dopamine depletion in the classical rat model of Parkinson's disease. They support the assumption that in addition to its action in the striatum, dopamine mediates its regulatory function at various levels of the basal ganglia circuitry, including the GP.
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| NO : | PASCAL 13-0158218 INIST |
|---|---|
| ET : | INTRAPALLIDAL ADMINISTRATION OF 6-HYDROXYDOPAMINE MIMICS IN LARGE PART THE ELECTROPHYSIOLOGICAL AND BEHAVIORAL CONSEQUENCES OF MAJOR DOPAMINE DEPLETION IN THE RAT |
| AU : | ABEDI (P. M.); DELAVILLE (C.); DE DEURWAERDERE (P.); BENJELLOUN (W.); BENAZZOUZ (A.) |
| AF : | Univ. Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293/33000 Bordeaux/France (1 aut., 2 aut., 3 aut., 5 aut.); Centre National de la Recherche Scientifique, Institut des Maladies Neurodégénératives, UMR 5293/33000 Bordeaux/France (1 aut., 2 aut., 3 aut., 5 aut.); Unité Neurosciences et Cognition, Faculté des Sciences, Université Mohammed V-Agdal/Rabat/Maroc (1 aut., 4 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | Neuroscience; ISSN 0306-4522; Coden NRSCDN; Pays-Bas; Da. 2013; Vol. 236; Pp. 289-297; Bibl. 1 p.3/4 |
| LA : | Anglais |
| EA : | In addition to GABA and glutamate innervations, the globus pallidus (GP) receives dopamine afferents from the pars compacta of the substantia nigra (SNc), and in turn, sends inhibitory GABAergic efferents to the subthalamic nucleus (STN) and the pars reticulata of the substantia nigra (SNr). Nevertheless, the role of dopamine in the modulation of these pallido-subthalamic and pallido-nigral projections is not known. The present study aimed to investigate the effects of intrapallidal injection of 6-hydroxydopamine (6-OHDA) on the electrical activity of STN and SNr neurons using in vivo extracellular single unit recordings in the rat and on motor behaviors, using the "open field" actimeter and the stepping test. We show that intrapallidal injection of 6-OHDA significantly decreased locomotor activity and contralateral paw use. Electrophysiological recordings show that 6-OHDA injection into GP significantly increased the number of bursty cells in the STN without changing the firing rate, while in the SNr neuronal firing rate decreased and the proportion of irregular cells increased. Our data provide evidence that intrapallidal injection of 6-OHDA resulted in motor deficits paralleled by changes in the firing activity of STN and SNr neurons, which mimic in large part those obtained after major dopamine depletion in the classical rat model of Parkinson's disease. They support the assumption that in addition to its action in the striatum, dopamine mediates its regulatory function at various levels of the basal ganglia circuitry, including the GP. |
| CC : | 002B17G; 002B17A01 |
| FD : | Oxidopamine; Electrophysiologie; Comportement; Dopamine; Déplétion; Pallidum; Noyau sousthalamique; Locus niger; Maladie de Parkinson; Rat; Animal |
| FG : | Catécholamine; Neurotransmetteur; Maladie dégénérative; Pathologie du système nerveux; Pathologie de l'encéphale; Syndrome extrapyramidal; Pathologie du système nerveux central; Encéphale; Noyau gris central; Système nerveux central; Rodentia; Mammalia; Vertebrata |
| ED : | Oxidopamine; Electrophysiology; Behavior; Dopamine; Depletion; Pallidum; Subthalamic nucleus; Locus niger; Parkinson disease; Rat; Animal |
| EG : | Catecholamine; Neurotransmitter; Degenerative disease; Nervous system diseases; Cerebral disorder; Extrapyramidal syndrome; Central nervous system disease; Encephalon; Basal ganglion; Central nervous system; Rodentia; Mammalia; Vertebrata |
| SD : | Oxidopamina; Electrofisiología; Conducta; Dopamina; Depleción; Pallidum; Núcleo subtalámico; Locus níger; Parkinson enfermedad; Rata; Animal |
| LO : | INIST-17194.354000500604180260 |
| ID : | 13-0158218 |
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Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293</s1><s2>33000 Bordeaux</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Centre National de la Recherche Scientifique, Institut des Maladies Neurodégénératives, UMR 5293</s1><s2>33000 Bordeaux</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">13-0158218</idno><date when="2013">2013</date><idno type="stanalyst">PASCAL 13-0158218 INIST</idno><idno type="RBID">Pascal:13-0158218</idno><idno type="wicri:Area/PascalFrancis/Corpus">000114</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">INTRAPALLIDAL ADMINISTRATION OF 6-HYDROXYDOPAMINE MIMICS IN LARGE PART THE ELECTROPHYSIOLOGICAL AND BEHAVIORAL CONSEQUENCES OF MAJOR DOPAMINE DEPLETION IN THE RAT</title><author><name sortKey="Abedi, P M" sort="Abedi, P M" uniqKey="Abedi P" first="P. M." last="Abedi">P. M. Abedi</name><affiliation><inist:fA14 i1="01"><s1>Univ. Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293</s1><s2>33000 Bordeaux</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Centre National de la Recherche Scientifique, Institut des Maladies Neurodégénératives, UMR 5293</s1><s2>33000 Bordeaux</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>Unité Neurosciences et Cognition, Faculté des Sciences, Université Mohammed V-Agdal</s1><s2>Rabat</s2><s3>MAR</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Delaville, C" sort="Delaville, C" uniqKey="Delaville C" first="C." last="Delaville">C. Delaville</name><affiliation><inist:fA14 i1="01"><s1>Univ. Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293</s1><s2>33000 Bordeaux</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Centre National de la Recherche Scientifique, Institut des Maladies Neurodégénératives, UMR 5293</s1><s2>33000 Bordeaux</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="De Deurwaerdere, P" sort="De Deurwaerdere, P" uniqKey="De Deurwaerdere P" first="P." last="De Deurwaerdere">P. De Deurwaerdere</name><affiliation><inist:fA14 i1="01"><s1>Univ. Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293</s1><s2>33000 Bordeaux</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Centre National de la Recherche Scientifique, Institut des Maladies Neurodégénératives, UMR 5293</s1><s2>33000 Bordeaux</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Benjelloun, W" sort="Benjelloun, W" uniqKey="Benjelloun W" first="W." last="Benjelloun">W. Benjelloun</name><affiliation><inist:fA14 i1="03"><s1>Unité Neurosciences et Cognition, Faculté des Sciences, Université Mohammed V-Agdal</s1><s2>Rabat</s2><s3>MAR</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Benazzouz, A" sort="Benazzouz, A" uniqKey="Benazzouz A" first="A." last="Benazzouz">A. Benazzouz</name><affiliation><inist:fA14 i1="01"><s1>Univ. Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293</s1><s2>33000 Bordeaux</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Centre National de la Recherche Scientifique, Institut des Maladies Neurodégénératives, UMR 5293</s1><s2>33000 Bordeaux</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">Neuroscience</title><title level="j" type="abbreviated">Neuroscience</title><idno type="ISSN">0306-4522</idno><imprint><date when="2013">2013</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Neuroscience</title><title level="j" type="abbreviated">Neuroscience</title><idno type="ISSN">0306-4522</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal</term><term>Behavior</term><term>Depletion</term><term>Dopamine</term><term>Electrophysiology</term><term>Locus niger</term><term>Oxidopamine</term><term>Pallidum</term><term>Parkinson disease</term><term>Rat</term><term>Subthalamic nucleus</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Oxidopamine</term><term>Electrophysiologie</term><term>Comportement</term><term>Dopamine</term><term>Déplétion</term><term>Pallidum</term><term>Noyau sousthalamique</term><term>Locus niger</term><term>Maladie de Parkinson</term><term>Rat</term><term>Animal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In addition to GABA and glutamate innervations, the globus pallidus (GP) receives dopamine afferents from the pars compacta of the substantia nigra (SNc), and in turn, sends inhibitory GABAergic efferents to the subthalamic nucleus (STN) and the pars reticulata of the substantia nigra (SNr). Nevertheless, the role of dopamine in the modulation of these pallido-subthalamic and pallido-nigral projections is not known. The present study aimed to investigate the effects of intrapallidal injection of 6-hydroxydopamine (6-OHDA) on the electrical activity of STN and SNr neurons using in vivo extracellular single unit recordings in the rat and on motor behaviors, using the "open field" actimeter and the stepping test. We show that intrapallidal injection of 6-OHDA significantly decreased locomotor activity and contralateral paw use. Electrophysiological recordings show that 6-OHDA injection into GP significantly increased the number of bursty cells in the STN without changing the firing rate, while in the SNr neuronal firing rate decreased and the proportion of irregular cells increased. Our data provide evidence that intrapallidal injection of 6-OHDA resulted in motor deficits paralleled by changes in the firing activity of STN and SNr neurons, which mimic in large part those obtained after major dopamine depletion in the classical rat model of Parkinson's disease. They support the assumption that in addition to its action in the striatum, dopamine mediates its regulatory function at various levels of the basal ganglia circuitry, including the GP.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0306-4522</s0></fA01><fA02 i1="01"><s0>NRSCDN</s0></fA02><fA03 i2="1"><s0>Neuroscience</s0></fA03><fA05><s2>236</s2></fA05><fA08 i1="01" i2="1" l="ENG"><s1>INTRAPALLIDAL ADMINISTRATION OF 6-HYDROXYDOPAMINE MIMICS IN LARGE PART THE ELECTROPHYSIOLOGICAL AND BEHAVIORAL CONSEQUENCES OF MAJOR DOPAMINE DEPLETION IN THE RAT</s1></fA08><fA11 i1="01" i2="1"><s1>ABEDI (P. M.)</s1></fA11><fA11 i1="02" i2="1"><s1>DELAVILLE (C.)</s1></fA11><fA11 i1="03" i2="1"><s1>DE DEURWAERDERE (P.)</s1></fA11><fA11 i1="04" i2="1"><s1>BENJELLOUN (W.)</s1></fA11><fA11 i1="05" i2="1"><s1>BENAZZOUZ (A.)</s1></fA11><fA14 i1="01"><s1>Univ. Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293</s1><s2>33000 Bordeaux</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></fA14><fA14 i1="02"><s1>Centre National de la Recherche Scientifique, Institut des Maladies Neurodégénératives, UMR 5293</s1><s2>33000 Bordeaux</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></fA14><fA14 i1="03"><s1>Unité Neurosciences et Cognition, Faculté des Sciences, Université Mohammed V-Agdal</s1><s2>Rabat</s2><s3>MAR</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ></fA14><fA20><s1>289-297</s1></fA20><fA21><s1>2013</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>17194</s2><s5>354000500604180260</s5></fA43><fA44><s0>0000</s0><s1>© 2013 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>1 p.3/4</s0></fA45><fA47 i1="01" i2="1"><s0>13-0158218</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Neuroscience</s0></fA64><fA66 i1="01"><s0>NLD</s0></fA66><fC01 i1="01" l="ENG"><s0>In addition to GABA and glutamate innervations, the globus pallidus (GP) receives dopamine afferents from the pars compacta of the substantia nigra (SNc), and in turn, sends inhibitory GABAergic efferents to the subthalamic nucleus (STN) and the pars reticulata of the substantia nigra (SNr). Nevertheless, the role of dopamine in the modulation of these pallido-subthalamic and pallido-nigral projections is not known. The present study aimed to investigate the effects of intrapallidal injection of 6-hydroxydopamine (6-OHDA) on the electrical activity of STN and SNr neurons using in vivo extracellular single unit recordings in the rat and on motor behaviors, using the "open field" actimeter and the stepping test. We show that intrapallidal injection of 6-OHDA significantly decreased locomotor activity and contralateral paw use. Electrophysiological recordings show that 6-OHDA injection into GP significantly increased the number of bursty cells in the STN without changing the firing rate, while in the SNr neuronal firing rate decreased and the proportion of irregular cells increased. Our data provide evidence that intrapallidal injection of 6-OHDA resulted in motor deficits paralleled by changes in the firing activity of STN and SNr neurons, which mimic in large part those obtained after major dopamine depletion in the classical rat model of Parkinson's disease. They support the assumption that in addition to its action in the striatum, dopamine mediates its regulatory function at various levels of the basal ganglia circuitry, including the GP.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17G</s0></fC02><fC02 i1="02" i2="X"><s0>002B17A01</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Oxidopamine</s0><s2>NK</s2><s2>FR</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Oxidopamine</s0><s2>NK</s2><s2>FR</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Oxidopamina</s0><s2>NK</s2><s2>FR</s2><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Electrophysiologie</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Electrophysiology</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Electrofisiología</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Comportement</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Behavior</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Conducta</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" 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i2="X" l="SPA"><s0>Locus níger</s0><s5>08</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>Maladie de Parkinson</s0><s2>NM</s2><s5>09</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>Parkinson disease</s0><s2>NM</s2><s5>09</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Parkinson enfermedad</s0><s2>NM</s2><s5>09</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Rat</s0><s5>54</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Rat</s0><s5>54</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Rata</s0><s5>54</s5></fC03><fC03 i1="11" i2="X" l="FRE"><s0>Animal</s0><s5>69</s5></fC03><fC03 i1="11" i2="X" l="ENG"><s0>Animal</s0><s5>69</s5></fC03><fC03 i1="11" i2="X" l="SPA"><s0>Animal</s0><s5>69</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Catécholamine</s0><s5>20</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Catecholamine</s0><s5>20</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Catecolamina</s0><s5>20</s5></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Neurotransmetteur</s0><s5>21</s5></fC07><fC07 i1="02" i2="X" 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i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>25</s5></fC07><fC07 i1="07" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0><s5>26</s5></fC07><fC07 i1="07" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>26</s5></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>26</s5></fC07><fC07 i1="08" i2="X" l="FRE"><s0>Encéphale</s0><s5>27</s5></fC07><fC07 i1="08" i2="X" l="ENG"><s0>Encephalon</s0><s5>27</s5></fC07><fC07 i1="08" i2="X" l="SPA"><s0>Encéfalo</s0><s5>27</s5></fC07><fC07 i1="09" i2="X" l="FRE"><s0>Noyau gris central</s0><s5>28</s5></fC07><fC07 i1="09" i2="X" l="ENG"><s0>Basal ganglion</s0><s5>28</s5></fC07><fC07 i1="09" i2="X" l="SPA"><s0>Núcleo basal</s0><s5>28</s5></fC07><fC07 i1="10" i2="X" l="FRE"><s0>Système nerveux central</s0><s5>29</s5></fC07><fC07 i1="10" i2="X" l="ENG"><s0>Central nervous system</s0><s5>29</s5></fC07><fC07 i1="10" i2="X" l="SPA"><s0>Sistema nervioso central</s0><s5>29</s5></fC07><fC07 i1="11" i2="X" l="FRE"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="11" i2="X" l="ENG"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="11" i2="X" l="SPA"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="12" i2="X" l="FRE"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="12" i2="X" l="ENG"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="12" i2="X" l="SPA"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="13" i2="X" l="FRE"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="13" i2="X" l="ENG"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="13" i2="X" l="SPA"><s0>Vertebrata</s0><s2>NS</s2></fC07><fN21><s1>140</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>PASCAL 13-0158218 INIST</NO><ET>INTRAPALLIDAL ADMINISTRATION OF 6-HYDROXYDOPAMINE MIMICS IN LARGE PART THE ELECTROPHYSIOLOGICAL AND BEHAVIORAL CONSEQUENCES OF MAJOR DOPAMINE DEPLETION IN THE RAT</ET><AU>ABEDI (P. M.); DELAVILLE (C.); DE DEURWAERDERE (P.); BENJELLOUN (W.); BENAZZOUZ (A.)</AU><AF>Univ. Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293/33000 Bordeaux/France (1 aut., 2 aut., 3 aut., 5 aut.); Centre National de la Recherche Scientifique, Institut des Maladies Neurodégénératives, UMR 5293/33000 Bordeaux/France (1 aut., 2 aut., 3 aut., 5 aut.); Unité Neurosciences et Cognition, Faculté des Sciences, Université Mohammed V-Agdal/Rabat/Maroc (1 aut., 4 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>Neuroscience; ISSN 0306-4522; Coden NRSCDN; Pays-Bas; Da. 2013; Vol. 236; Pp. 289-297; Bibl. 1 p.3/4</SO><LA>Anglais</LA><EA>In addition to GABA and glutamate innervations, the globus pallidus (GP) receives dopamine afferents from the pars compacta of the substantia nigra (SNc), and in turn, sends inhibitory GABAergic efferents to the subthalamic nucleus (STN) and the pars reticulata of the substantia nigra (SNr). Nevertheless, the role of dopamine in the modulation of these pallido-subthalamic and pallido-nigral projections is not known. The present study aimed to investigate the effects of intrapallidal injection of 6-hydroxydopamine (6-OHDA) on the electrical activity of STN and SNr neurons using in vivo extracellular single unit recordings in the rat and on motor behaviors, using the "open field" actimeter and the stepping test. We show that intrapallidal injection of 6-OHDA significantly decreased locomotor activity and contralateral paw use. Electrophysiological recordings show that 6-OHDA injection into GP significantly increased the number of bursty cells in the STN without changing the firing rate, while in the SNr neuronal firing rate decreased and the proportion of irregular cells increased. Our data provide evidence that intrapallidal injection of 6-OHDA resulted in motor deficits paralleled by changes in the firing activity of STN and SNr neurons, which mimic in large part those obtained after major dopamine depletion in the classical rat model of Parkinson's disease. They support the assumption that in addition to its action in the striatum, dopamine mediates its regulatory function at various levels of the basal ganglia circuitry, including the GP.</EA><CC>002B17G; 002B17A01</CC><FD>Oxidopamine; Electrophysiologie; Comportement; Dopamine; Déplétion; Pallidum; Noyau sousthalamique; Locus niger; Maladie de Parkinson; Rat; Animal</FD><FG>Catécholamine; Neurotransmetteur; Maladie dégénérative; Pathologie du système nerveux; Pathologie de l'encéphale; Syndrome extrapyramidal; Pathologie du système nerveux central; Encéphale; Noyau gris central; Système nerveux central; Rodentia; Mammalia; Vertebrata</FG><ED>Oxidopamine; Electrophysiology; Behavior; Dopamine; Depletion; Pallidum; Subthalamic nucleus; Locus niger; Parkinson disease; Rat; Animal</ED><EG>Catecholamine; Neurotransmitter; Degenerative disease; Nervous system diseases; Cerebral disorder; Extrapyramidal syndrome; Central nervous system disease; Encephalon; Basal ganglion; Central nervous system; Rodentia; Mammalia; Vertebrata</EG><SD>Oxidopamina; Electrofisiología; Conducta; Dopamina; Depleción; Pallidum; Núcleo subtalámico; Locus níger; Parkinson enfermedad; Rata; Animal</SD><LO>INIST-17194.354000500604180260</LO><ID>13-0158218</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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