Absence of MPTP-lnduced neuronal death in mice lacking the dopamine transporter
Identifieur interne : 001368 ( PascalFrancis/Checkpoint ); précédent : 001367; suivant : 001369Absence of MPTP-lnduced neuronal death in mice lacking the dopamine transporter
Auteurs : E. Bezard [France] ; C. E. Gross [France] ; M.-C. Fournier [France] ; S. Dovero [France] ; B. Bloch [France] ; M. Jaber [France]Source :
- Experimental neurology [ 0014-4886 ] ; 1999.
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Abstract
MPTP has been shown to induce parkinsonism both in human and in nonhuman primates. The precise mechanism of dopaminergic cell death induced following MPTP treatment is still subject to intense debate. MPP+, which is the oxidation product of MPTP, is actively transported into presynaptic dopaminergic nerve terminals through the plasma membrane dopamine transporter (DAT). In this study, we used mice lacking the DAT by homologous recombination and demonstrated that the MPTP-induced dopaminergic cell loss is dependent on the presence of the DAT. For this we have used tyrosine hydroxylase immunoreactivity (TH-IR) labeling of dopamine cells of the substantia nigra compacta in wild-type, heterozygote, and homozygote mice that were given either saline or MPTP treatments (two ip injections of 30 mg/kg, 10 h apart). Our results show a significant loss of TH-IR in wild type (34.4%), less loss in heterozygotes (22.5%), and no loss in homozygote animals. Thus dopamine cell loss is related to levels of the DAT. These results shed light on the degenerative process of dopamine neurons and suggest that individual differences in developing Parkinson's disease in human may be related to differences of uptake through the DAT of a yet unidentified neurotoxin.
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Bezard</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>Basal Gang, Laboratoire de Neurophysiologie, CNRS UMR 5543</s1><s2>33076 Bordeaux</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region" nuts="2">Nouvelle-Aquitaine</region><region type="old region" nuts="2">Aquitaine</region><settlement type="city">Bordeaux</settlement></placeName></affiliation></author><author><name sortKey="Gross, C E" sort="Gross, C E" uniqKey="Gross C" first="C. E." last="Gross">C. E. Gross</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>Basal Gang, Laboratoire de Neurophysiologie, CNRS UMR 5543</s1><s2>33076 Bordeaux</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region" nuts="2">Nouvelle-Aquitaine</region><region type="old region" nuts="2">Aquitaine</region><settlement type="city">Bordeaux</settlement></placeName></affiliation></author><author><name sortKey="Fournier, M C" sort="Fournier, M C" uniqKey="Fournier M" first="M.-C." last="Fournier">M.-C. Fournier</name><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>CNRS UMR 5541, Université de Bordeaux II, 146 rue Leo Saignat</s1><s2>33076 Bordeaux</s2><s3>FRA</s3><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region" nuts="2">Nouvelle-Aquitaine</region><region type="old region" nuts="2">Aquitaine</region><settlement type="city">Bordeaux</settlement></placeName></affiliation></author><author><name sortKey="Dovero, S" sort="Dovero, S" uniqKey="Dovero S" first="S." last="Dovero">S. Dovero</name><affiliation wicri:level="3"><inist:fA14 i1="01"><s1>Basal Gang, Laboratoire de Neurophysiologie, CNRS UMR 5543</s1><s2>33076 Bordeaux</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region" nuts="2">Nouvelle-Aquitaine</region><region type="old region" nuts="2">Aquitaine</region><settlement type="city">Bordeaux</settlement></placeName></affiliation></author><author><name sortKey="Bloch, B" sort="Bloch, B" uniqKey="Bloch B" first="B." last="Bloch">B. Bloch</name><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>CNRS UMR 5541, Université de Bordeaux II, 146 rue Leo Saignat</s1><s2>33076 Bordeaux</s2><s3>FRA</s3><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region" nuts="2">Nouvelle-Aquitaine</region><region type="old region" nuts="2">Aquitaine</region><settlement type="city">Bordeaux</settlement></placeName></affiliation></author><author><name sortKey="Jaber, M" sort="Jaber, M" uniqKey="Jaber M" first="M." last="Jaber">M. Jaber</name><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>CNRS UMR 5541, Université de Bordeaux II, 146 rue Leo Saignat</s1><s2>33076 Bordeaux</s2><s3>FRA</s3><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region" nuts="2">Nouvelle-Aquitaine</region><region type="old region" nuts="2">Aquitaine</region><settlement type="city">Bordeaux</settlement></placeName></affiliation></author></analytic><series><title level="j" type="main">Experimental neurology</title><title level="j" type="abbreviated">Exp. neurol.</title><idno type="ISSN">0014-4886</idno><imprint><date when="1999">1999</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Experimental neurology</title><title level="j" type="abbreviated">Exp. neurol.</title><idno type="ISSN">0014-4886</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal</term><term>Animal model</term><term>Biological transport</term><term>Cell death</term><term>Conveyor</term><term>Deficiency</term><term>Dopamine</term><term>Dopaminergic neuron</term><term>Mouse</term><term>Neurotoxin</term><term>Parkinson disease</term><term>Pathogenesis</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Déficit</term><term>Transporteur</term><term>Dopamine</term><term>Transport biologique</term><term>Parkinson maladie</term><term>Neurone dopaminergique</term><term>Neurotoxine</term><term>Pyridine(1-méthyl-4-phényl-1,2,3,6-tétrahydro)</term><term>Pathogénie</term><term>Modèle animal</term><term>Animal</term><term>Souris</term><term>Mort cellulaire</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Déficit</term><term>Transporteur</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">MPTP has been shown to induce parkinsonism both in human and in nonhuman primates. The precise mechanism of dopaminergic cell death induced following MPTP treatment is still subject to intense debate. MPP<sup>+</sup>, which is the oxidation product of MPTP, is actively transported into presynaptic dopaminergic nerve terminals through the plasma membrane dopamine transporter (DAT). In this study, we used mice lacking the DAT by homologous recombination and demonstrated that the MPTP-induced dopaminergic cell loss is dependent on the presence of the DAT. For this we have used tyrosine hydroxylase immunoreactivity (TH-IR) labeling of dopamine cells of the substantia nigra compacta in wild-type, heterozygote, and homozygote mice that were given either saline or MPTP treatments (two ip injections of 30 mg/kg, 10 h apart). Our results show a significant loss of TH-IR in wild type (34.4%), less loss in heterozygotes (22.5%), and no loss in homozygote animals. Thus dopamine cell loss is related to levels of the DAT. These results shed light on the degenerative process of dopamine neurons and suggest that individual differences in developing Parkinson's disease in human may be related to differences of uptake through the DAT of a yet unidentified neurotoxin.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0014-4886</s0></fA01><fA02 i1="01"><s0>EXNEAC</s0></fA02><fA03 i2="1"><s0>Exp. neurol.</s0></fA03><fA05><s2>155</s2></fA05><fA06><s2>2</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Absence of MPTP-lnduced neuronal death in mice lacking the dopamine transporter</s1></fA08><fA11 i1="01" i2="1"><s1>BEZARD (E.)</s1></fA11><fA11 i1="02" i2="1"><s1>GROSS (C. E.)</s1></fA11><fA11 i1="03" i2="1"><s1>FOURNIER (M.-C.)</s1></fA11><fA11 i1="04" i2="1"><s1>DOVERO (S.)</s1></fA11><fA11 i1="05" i2="1"><s1>BLOCH (B.)</s1></fA11><fA11 i1="06" i2="1"><s1>JABER (M.)</s1></fA11><fA14 i1="01"><s1>Basal Gang, Laboratoire de Neurophysiologie, CNRS UMR 5543</s1><s2>33076 Bordeaux</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ></fA14><fA14 i1="02"><s1>CNRS UMR 5541, Université de Bordeaux II, 146 rue Leo Saignat</s1><s2>33076 Bordeaux</s2><s3>FRA</s3><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></fA14><fA20><s1>268-273</s1></fA20><fA21><s1>1999</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>9181</s2><s5>354000073981760110</s5></fA43><fA44><s0>0000</s0><s1>© 1999 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>38 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>99-0219067</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Experimental neurology</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>MPTP has been shown to induce parkinsonism both in human and in nonhuman primates. The precise mechanism of dopaminergic cell death induced following MPTP treatment is still subject to intense debate. MPP<sup>+</sup>, which is the oxidation product of MPTP, is actively transported into presynaptic dopaminergic nerve terminals through the plasma membrane dopamine transporter (DAT). In this study, we used mice lacking the DAT by homologous recombination and demonstrated that the MPTP-induced dopaminergic cell loss is dependent on the presence of the DAT. For this we have used tyrosine hydroxylase immunoreactivity (TH-IR) labeling of dopamine cells of the substantia nigra compacta in wild-type, heterozygote, and homozygote mice that were given either saline or MPTP treatments (two ip injections of 30 mg/kg, 10 h apart). Our results show a significant loss of TH-IR in wild type (34.4%), less loss in heterozygotes (22.5%), and no loss in homozygote animals. Thus dopamine cell loss is related to levels of the DAT. These results shed light on the degenerative process of dopamine neurons and suggest that individual differences in developing Parkinson's disease in human may be related to differences of uptake through the DAT of a yet unidentified neurotoxin.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17G</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Déficit</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Deficiency</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Déficiencia</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Transporteur</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Conveyor</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Transportador</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Dopamine</s0><s2>NK</s2><s2>FR</s2><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Dopamine</s0><s2>NK</s2><s2>FR</s2><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Dopamina</s0><s2>NK</s2><s2>FR</s2><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Transport 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Bezard</name></region><name sortKey="Bloch, B" sort="Bloch, B" uniqKey="Bloch B" first="B." last="Bloch">B. Bloch</name><name sortKey="Dovero, S" sort="Dovero, S" uniqKey="Dovero S" first="S." last="Dovero">S. Dovero</name><name sortKey="Fournier, M C" sort="Fournier, M C" uniqKey="Fournier M" first="M.-C." last="Fournier">M.-C. Fournier</name><name sortKey="Gross, C E" sort="Gross, C E" uniqKey="Gross C" first="C. E." last="Gross">C. E. Gross</name><name sortKey="Jaber, M" sort="Jaber, M" uniqKey="Jaber M" first="M." last="Jaber">M. Jaber</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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