Levodopa‐induced dyskinesia in MPTP‐treated macaques is not dependent on the extent and pattern of nigrostrial lesioning
Identifieur interne : 000D48 ( Istex/Corpus ); précédent : 000D47; suivant : 000D49Levodopa‐induced dyskinesia in MPTP‐treated macaques is not dependent on the extent and pattern of nigrostrial lesioning
Auteurs : Céline Guigoni ; Sandra Dovero ; Incarnation Aubert ; Qin Li ; Bernard H. Bioulac ; Bertrand Bloch ; Eugenia V. Gurevich ; Christian E. Gross ; Erwan BezardSource :
- European Journal of Neuroscience [ 0953-816X ] ; 2005-07.
English descriptors
Abstract
The extent of nigrostriatal denervation is presumed to play a role in the genesis of levodopa‐induced dyskinesia. Yet some parkinsonian patients who have been treated over a long period do not develop dyskinesia, raising the possibility that the pattern of denervation is as important as the extent of lesioning as a risk factor. Here we study the extent and pattern of nigrostriatal denervation in a homogeneous population of parkinsonian macaque monkeys chronically treated with levodopa. Based on the characteristics of the lesioning, non‐dyskinetic animals could not be differentiated from those with dyskinesia. Indeed, the number of tyrosine‐hydroxylase (TH)‐immunopositive neurons in the substantia nigra pars compacta, striatal dopamine transporter (DAT) binding and TH immunostaining, as well as the overall TH striatal content measured by Western blotting were identical. Moreover, the patterns of lesioning assessed by a detailed analysis of the TH‐ and DAT‐immunopositive striatal fibers were comparable in all functional quadrants and at all rostro‐caudal levels considered. These data indicate that neither the extent nor the pattern of nigrostriatal lesioning are sufficient to explain the occurrence of levodopa‐induced dyskinesia.
Url:
DOI: 10.1111/j.1460-9568.2005.04196.x
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<front><div type="abstract" xml:lang="en">The extent of nigrostriatal denervation is presumed to play a role in the genesis of levodopa‐induced dyskinesia. Yet some parkinsonian patients who have been treated over a long period do not develop dyskinesia, raising the possibility that the pattern of denervation is as important as the extent of lesioning as a risk factor. Here we study the extent and pattern of nigrostriatal denervation in a homogeneous population of parkinsonian macaque monkeys chronically treated with levodopa. Based on the characteristics of the lesioning, non‐dyskinetic animals could not be differentiated from those with dyskinesia. Indeed, the number of tyrosine‐hydroxylase (TH)‐immunopositive neurons in the substantia nigra pars compacta, striatal dopamine transporter (DAT) binding and TH immunostaining, as well as the overall TH striatal content measured by Western blotting were identical. Moreover, the patterns of lesioning assessed by a detailed analysis of the TH‐ and DAT‐immunopositive striatal fibers were comparable in all functional quadrants and at all rostro‐caudal levels considered. These data indicate that neither the extent nor the pattern of nigrostriatal lesioning are sufficient to explain the occurrence of levodopa‐induced dyskinesia.</div>
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<author xml:id="author-1"><persName><forename type="first">Céline</forename>
<surname>Guigoni</surname>
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<affiliation>Laboratoire de Physiologie et Physiopathologie de la Signalization Cellulaire, CNRS UMR 5543,</affiliation>
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<author xml:id="author-2"><persName><forename type="first">Sandra</forename>
<surname>Dovero</surname>
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<affiliation>Laboratoire de Physiologie et Physiopathologie de la Signalization Cellulaire, CNRS UMR 5543,</affiliation>
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<author xml:id="author-3"><persName><forename type="first">Incarnation</forename>
<surname>Aubert</surname>
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<affiliation>CNRS UMR 5541, Université Victor Segalen‐Bordeaux 2, 146 rue Léo Saignat, 33076 Bordeaux Cedex, France</affiliation>
</author>
<author xml:id="author-4"><persName><forename type="first">Qin</forename>
<surname>Li</surname>
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<affiliation>Laboratory Animal Research Centre, China Agricultural University, Beijing, China</affiliation>
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<author xml:id="author-5"><persName><forename type="first">Bernard H.</forename>
<surname>Bioulac</surname>
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<affiliation>Laboratoire de Physiologie et Physiopathologie de la Signalization Cellulaire, CNRS UMR 5543,</affiliation>
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<author xml:id="author-6"><persName><forename type="first">Bertrand</forename>
<surname>Bloch</surname>
</persName>
<affiliation>CNRS UMR 5541, Université Victor Segalen‐Bordeaux 2, 146 rue Léo Saignat, 33076 Bordeaux Cedex, France</affiliation>
</author>
<author xml:id="author-7"><persName><forename type="first">Eugenia V.</forename>
<surname>Gurevich</surname>
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<affiliation>Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232, USA</affiliation>
</author>
<author xml:id="author-8"><persName><forename type="first">Christian E.</forename>
<surname>Gross</surname>
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<affiliation>Laboratoire de Physiologie et Physiopathologie de la Signalization Cellulaire, CNRS UMR 5543,</affiliation>
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<author xml:id="author-9"><persName><forename type="first">Erwan</forename>
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<abstract xml:lang="en"><p>The extent of nigrostriatal denervation is presumed to play a role in the genesis of levodopa‐induced dyskinesia. Yet some parkinsonian patients who have been treated over a long period do not develop dyskinesia, raising the possibility that the pattern of denervation is as important as the extent of lesioning as a risk factor. Here we study the extent and pattern of nigrostriatal denervation in a homogeneous population of parkinsonian macaque monkeys chronically treated with levodopa. Based on the characteristics of the lesioning, non‐dyskinetic animals could not be differentiated from those with dyskinesia. Indeed, the number of tyrosine‐hydroxylase (TH)‐immunopositive neurons in the substantia nigra pars compacta, striatal dopamine transporter (DAT) binding and TH immunostaining, as well as the overall TH striatal content measured by Western blotting were identical. Moreover, the patterns of lesioning assessed by a detailed analysis of the TH‐ and DAT‐immunopositive striatal fibers were comparable in all functional quadrants and at all rostro‐caudal levels considered. These data indicate that neither the extent nor the pattern of nigrostriatal lesioning are sufficient to explain the occurrence of levodopa‐induced dyskinesia.</p>
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<item><term>dopamine transporter</term>
</item>
<item><term>Parkinson's disease</term>
</item>
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<correspondenceTo>Dr E. Bezard, as above.
E‐mail: <email normalForm="erwan.bezard@umr5543.u-bordeaux2.fr">erwan.bezard@umr5543.u‐bordeaux2.fr</email>
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<contentMeta><unparsedEditorialHistory>Received 9 March 2005, revised 13 April 2005, accepted 9 May 2005</unparsedEditorialHistory>
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<titleGroup><title type="main">Levodopa‐induced dyskinesia in MPTP‐treated macaques is not dependent on the extent and pattern of nigrostrial lesioning</title>
<title type="shortAuthors">C. Guigoni <i>et al.</i>
</title>
<title type="short">Dyskinesia genesis and nigrostriatal lesion</title>
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<affiliation xml:id="a2" countryCode="FR"><unparsedAffiliation>CNRS UMR 5541, Université Victor Segalen‐Bordeaux 2, 146 rue Léo Saignat, 33076 Bordeaux Cedex, France</unparsedAffiliation>
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<affiliation xml:id="a3" countryCode="CN"><unparsedAffiliation>Laboratory Animal Research Centre, China Agricultural University, Beijing, China</unparsedAffiliation>
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<affiliation xml:id="a4" countryCode="US"><unparsedAffiliation>Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232, USA</unparsedAffiliation>
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<keywordGroup xml:lang="en"><keyword xml:id="k1">dopamine transporter</keyword>
<keyword xml:id="k2">Parkinson's disease</keyword>
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<keyword xml:id="k4">substantia nigra</keyword>
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<supportingInformation><p><b>Fig. S1.</b>
Pattern of lesion in control, MPTP‐lesioned untreated, MPTP‐lesioned LDOPA‐ treated non‐dyskinetic, and L‐DOPA‐treated dyskinetic monkeys. Representative high power photomicrographs of the striatal sections immunostained for TH shown in figure 1F (top row) and of adjacent striatal sections double‐immunolabelled (bottom) for TH (green) and DAT (red). Colocalisation of TH and DAT immunoreactivity produces a yellow signal. Scale bar = 55 ?m. Photomicrographs have been taken in all striatal quadrants at exactly the same position on each section to avoid selection bias: Cdl: caudate dorso‐lateral; Cdm: caudate dorso‐median; Cvl: caudate ventrolateral; Cvm: caudate ventro‐median; Pdl: putamen dorso‐lateral; Pdm: putamen dorso‐median; Pvl: putamen ventro‐lateral; Pvm: putamen ventro‐median.</p>
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<abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title>
<p>The extent of nigrostriatal denervation is presumed to play a role in the genesis of levodopa‐induced dyskinesia. Yet some parkinsonian patients who have been treated over a long period do not develop dyskinesia, raising the possibility that the pattern of denervation is as important as the extent of lesioning as a risk factor. Here we study the extent and pattern of nigrostriatal denervation in a homogeneous population of parkinsonian macaque monkeys chronically treated with levodopa. Based on the characteristics of the lesioning, non‐dyskinetic animals could not be differentiated from those with dyskinesia. Indeed, the number of tyrosine‐hydroxylase (TH)‐immunopositive neurons in the substantia nigra pars compacta, striatal dopamine transporter (DAT) binding and TH immunostaining, as well as the overall TH striatal content measured by Western blotting were identical. Moreover, the patterns of lesioning assessed by a detailed analysis of the TH‐ and DAT‐immunopositive striatal fibers were comparable in all functional quadrants and at all rostro‐caudal levels considered. These data indicate that neither the extent nor the pattern of nigrostriatal lesioning are sufficient to explain the occurrence of levodopa‐induced dyskinesia.</p>
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<mods version="3.6"><titleInfo lang="en"><title>Levodopa‐induced dyskinesia in MPTP‐treated macaques is not dependent on the extent and pattern of nigrostrial lesioning</title>
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<titleInfo type="abbreviated" lang="en"><title>Dyskinesia genesis and nigrostriatal lesion</title>
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<titleInfo type="alternative" contentType="CDATA" lang="en"><title>Levodopa‐induced dyskinesia in MPTP‐treated macaques is not dependent on the extent and pattern of nigrostrial lesioning</title>
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<name type="personal"><namePart type="given">Céline</namePart>
<namePart type="family">Guigoni</namePart>
<affiliation>Laboratoire de Physiologie et Physiopathologie de la Signalization Cellulaire, CNRS UMR 5543,</affiliation>
<role><roleTerm type="text">author</roleTerm>
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</name>
<name type="personal"><namePart type="given">Sandra</namePart>
<namePart type="family">Dovero</namePart>
<affiliation>Laboratoire de Physiologie et Physiopathologie de la Signalization Cellulaire, CNRS UMR 5543,</affiliation>
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<name type="personal"><namePart type="given">Incarnation</namePart>
<namePart type="family">Aubert</namePart>
<affiliation>CNRS UMR 5541, Université Victor Segalen‐Bordeaux 2, 146 rue Léo Saignat, 33076 Bordeaux Cedex, France</affiliation>
<role><roleTerm type="text">author</roleTerm>
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<name type="personal"><namePart type="given">Qin</namePart>
<namePart type="family">Li</namePart>
<affiliation>Laboratory Animal Research Centre, China Agricultural University, Beijing, China</affiliation>
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<name type="personal"><namePart type="given">Bernard H.</namePart>
<namePart type="family">Bioulac</namePart>
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<name type="personal"><namePart type="given">Bertrand</namePart>
<namePart type="family">Bloch</namePart>
<affiliation>CNRS UMR 5541, Université Victor Segalen‐Bordeaux 2, 146 rue Léo Saignat, 33076 Bordeaux Cedex, France</affiliation>
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<name type="personal"><namePart type="given">Eugenia V.</namePart>
<namePart type="family">Gurevich</namePart>
<affiliation>Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232, USA</affiliation>
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<name type="personal"><namePart type="given">Christian E.</namePart>
<namePart type="family">Gross</namePart>
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<name type="personal"><namePart type="given">Erwan</namePart>
<namePart type="family">Bezard</namePart>
<affiliation>Laboratoire de Physiologie et Physiopathologie de la Signalization Cellulaire, CNRS UMR 5543,</affiliation>
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<dateIssued encoding="w3cdtf">2005-07</dateIssued>
<edition>Received 9 March 2005, revised 13 April 2005, accepted 9 May 2005</edition>
<copyrightDate encoding="w3cdtf">2005</copyrightDate>
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<abstract lang="en">The extent of nigrostriatal denervation is presumed to play a role in the genesis of levodopa‐induced dyskinesia. Yet some parkinsonian patients who have been treated over a long period do not develop dyskinesia, raising the possibility that the pattern of denervation is as important as the extent of lesioning as a risk factor. Here we study the extent and pattern of nigrostriatal denervation in a homogeneous population of parkinsonian macaque monkeys chronically treated with levodopa. Based on the characteristics of the lesioning, non‐dyskinetic animals could not be differentiated from those with dyskinesia. Indeed, the number of tyrosine‐hydroxylase (TH)‐immunopositive neurons in the substantia nigra pars compacta, striatal dopamine transporter (DAT) binding and TH immunostaining, as well as the overall TH striatal content measured by Western blotting were identical. Moreover, the patterns of lesioning assessed by a detailed analysis of the TH‐ and DAT‐immunopositive striatal fibers were comparable in all functional quadrants and at all rostro‐caudal levels considered. These data indicate that neither the extent nor the pattern of nigrostriatal lesioning are sufficient to explain the occurrence of levodopa‐induced dyskinesia.</abstract>
<subject lang="en"><genre>keywords</genre>
<topic>dopamine transporter</topic>
<topic>Parkinson's disease</topic>
<topic>striatum</topic>
<topic>substantia nigra</topic>
<topic>tyrosine hydroxylase</topic>
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<relatedItem type="host"><titleInfo><title>European Journal of Neuroscience</title>
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<note type="content"> Fig. S1. Pattern of lesion in control, MPTP‐lesioned untreated, MPTP‐lesioned LDOPA‐ treated non‐dyskinetic, and L‐DOPA‐treated dyskinetic monkeys. Representative high power photomicrographs of the striatal sections immunostained for TH shown in figure 1F (top row) and of adjacent striatal sections double‐immunolabelled (bottom) for TH (green) and DAT (red). Colocalisation of TH and DAT immunoreactivity produces a yellow signal. Scale bar = 55 ?m. Photomicrographs have been taken in all striatal quadrants at exactly the same position on each section to avoid selection bias: Cdl: caudate dorso‐lateral; Cdm: caudate dorso‐median; Cvl: caudate ventrolateral; Cvm: caudate ventro‐median; Pdl: putamen dorso‐lateral; Pdm: putamen dorso‐median; Pvl: putamen ventro‐lateral; Pvm: putamen ventro‐median.Supporting Info Item: Supporting info item - </note>
<identifier type="ISSN">0953-816X</identifier>
<identifier type="eISSN">1460-9568</identifier>
<identifier type="DOI">10.1111/(ISSN)1460-9568</identifier>
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<part><date>2005</date>
<detail type="volume"><caption>vol.</caption>
<number>22</number>
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