Adaptive changes in the nigrostriatal pathway in response to increased 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurodegeneration in the mouse.
Identifieur interne : 000133 ( Ncbi/Curation ); précédent : 000132; suivant : 000134Adaptive changes in the nigrostriatal pathway in response to increased 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurodegeneration in the mouse.
Auteurs : E. Bezard [France] ; M. Jaber ; F. Gonon ; A. Boireau ; B. Bloch ; C E GrossSource :
- The European journal of neuroscience [ 0953-816X ] ; 2000.
English descriptors
- KwdEn :
- 3,4-Dihydroxyphenylacetic Acid (metabolism), Animals, Carrier Proteins (metabolism), Cell Count, Corpus Striatum (metabolism), Corpus Striatum (pathology), Disease Models, Animal, Dopamine (pharmacokinetics), Dopamine Plasma Membrane Transport Proteins, Electric Stimulation, Electron Transport Complex IV (metabolism), Electrophysiology, Homovanillic Acid (metabolism), MPTP Poisoning (metabolism), MPTP Poisoning (pathology), Male, Membrane Glycoproteins, Membrane Transport Proteins, Mice, Mice, Inbred Strains, Nerve Degeneration (chemically induced), Nerve Degeneration (metabolism), Nerve Degeneration (pathology), Nerve Tissue Proteins, Neurons (enzymology), Neurons (pathology), Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (metabolism), Parkinson Disease, Secondary (pathology), Substantia Nigra (metabolism), Substantia Nigra (pathology), Synaptosomes (metabolism), Tritium, Tyrosine 3-Monooxygenase (analysis).
- MESH :
- chemical , analysis : Tyrosine 3-Monooxygenase.
- chemical , metabolism : 3,4-Dihydroxyphenylacetic Acid, Carrier Proteins, Electron Transport Complex IV, Homovanillic Acid.
- chemically induced : Nerve Degeneration, Parkinson Disease, Secondary.
- enzymology : Neurons.
- metabolism : Corpus Striatum, MPTP Poisoning, Nerve Degeneration, Parkinson Disease, Secondary, Substantia Nigra, Synaptosomes.
- pathology : Corpus Striatum, MPTP Poisoning, Nerve Degeneration, Neurons, Parkinson Disease, Secondary, Substantia Nigra.
- chemical , pharmacokinetics : Dopamine.
- Animals, Cell Count, Disease Models, Animal, Dopamine Plasma Membrane Transport Proteins, Electric Stimulation, Electrophysiology, Male, Membrane Glycoproteins, Membrane Transport Proteins, Mice, Mice, Inbred Strains, Nerve Tissue Proteins, Tritium.
Abstract
Although several adaptive mechanisms have been identified that mask the existence of Parkinson's disease and delay the onset and aggravation of motor symptoms, the timescale and implications of this compensatory process remain an enigma. In order to examine: (i) the nature of the dopaminergic adaptive mechanisms that come into action; (ii) their sequential activation in relation to the severity of degeneration; and (iii) their efficacy with regard to the maintenance of a normal level of basal ganglia activity, we analysed the brains of mice treated daily with 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP, 4 mg/kg, i.p.) and killed at 5-day intervals from day 0 (D0) to D20. Our results demonstrate the sequential activation of two compensatory mechanisms: (i) an increase in striatal tyrosine hydroxylase (TH) protein content attested by the persistence of TH immunolabelling up to D15, contrasting with the decrease observed in both the number of nigral TH-immunoreactive neurons (-70.2%) and striatal dopamine content (-38.4%); (ii) a downregulation of DA uptake in surviving terminals at D20 (73.4% of nigral degeneration). At this point, the failure of adaptive mechanisms to maintain striatal dopaminergic homeostasis is also illustrated by an increase in the cytochrome oxidase activity of substantia nigra pars reticulata, a marker of neuronal function. It has been postulated that an increase in dopamine release per pulse could constitute an adaptive mechanism. The data we present from our MPTP mice model infirm this hypothesis. This study explores the link between the degree of nigral degeneration and the sequential activation of dopaminergic compensatory mechanisms in the nigrostriatal pathway and, in so doing, proposes a rethink of the paradigm applied to these mechanisms.
PubMed: 10971632
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Bezard</name><affiliation wicri:level="3"><nlm:affiliation>Basal Gang, Laboratoire de Neurophysiologie, CNRS UMR 5543, Université Victor Segalen, 146 rue Léo Saignat, 33076 Bordeaux Cedex, France. erwan.bezard@umr5543.u-bordeaux2.fr</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Basal Gang, Laboratoire de Neurophysiologie, CNRS UMR 5543, Université Victor Segalen, 146 rue Léo Saignat, 33076 Bordeaux Cedex</wicri:regionArea><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></author><author><name sortKey="Gonon, F" sort="Gonon, F" uniqKey="Gonon F" first="F" last="Gonon">F. Gonon</name></author><author><name sortKey="Boireau, A" sort="Boireau, A" uniqKey="Boireau A" first="A" last="Boireau">A. Boireau</name></author><author><name sortKey="Bloch, B" sort="Bloch, B" uniqKey="Bloch B" first="B" last="Bloch">B. Bloch</name></author><author><name sortKey="Gross, C E" sort="Gross, C E" uniqKey="Gross C" first="C E" last="Gross">C E Gross</name></author></analytic><series><title level="j">The European journal of neuroscience</title><idno type="ISSN">0953-816X</idno><imprint><date when="2000" type="published">2000</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>3,4-Dihydroxyphenylacetic Acid (metabolism)</term><term>Animals</term><term>Carrier Proteins (metabolism)</term><term>Cell Count</term><term>Corpus Striatum (metabolism)</term><term>Corpus Striatum (pathology)</term><term>Disease Models, Animal</term><term>Dopamine (pharmacokinetics)</term><term>Dopamine Plasma Membrane Transport Proteins</term><term>Electric Stimulation</term><term>Electron Transport Complex IV (metabolism)</term><term>Electrophysiology</term><term>Homovanillic Acid (metabolism)</term><term>MPTP Poisoning (metabolism)</term><term>MPTP Poisoning (pathology)</term><term>Male</term><term>Membrane Glycoproteins</term><term>Membrane Transport Proteins</term><term>Mice</term><term>Mice, Inbred Strains</term><term>Nerve Degeneration (chemically induced)</term><term>Nerve Degeneration (metabolism)</term><term>Nerve Degeneration (pathology)</term><term>Nerve Tissue Proteins</term><term>Neurons (enzymology)</term><term>Neurons (pathology)</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (metabolism)</term><term>Parkinson Disease, Secondary (pathology)</term><term>Substantia Nigra (metabolism)</term><term>Substantia Nigra (pathology)</term><term>Synaptosomes (metabolism)</term><term>Tritium</term><term>Tyrosine 3-Monooxygenase (analysis)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Tyrosine 3-Monooxygenase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>3,4-Dihydroxyphenylacetic Acid</term><term>Carrier Proteins</term><term>Electron Transport Complex IV</term><term>Homovanillic Acid</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Nerve Degeneration</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term><term>MPTP Poisoning</term><term>Nerve Degeneration</term><term>Parkinson Disease, Secondary</term><term>Substantia Nigra</term><term>Synaptosomes</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Corpus Striatum</term><term>MPTP Poisoning</term><term>Nerve Degeneration</term><term>Neurons</term><term>Parkinson Disease, Secondary</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Count</term><term>Disease Models, Animal</term><term>Dopamine Plasma Membrane Transport Proteins</term><term>Electric Stimulation</term><term>Electrophysiology</term><term>Male</term><term>Membrane Glycoproteins</term><term>Membrane Transport Proteins</term><term>Mice</term><term>Mice, Inbred Strains</term><term>Nerve Tissue Proteins</term><term>Tritium</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Although several adaptive mechanisms have been identified that mask the existence of Parkinson's disease and delay the onset and aggravation of motor symptoms, the timescale and implications of this compensatory process remain an enigma. In order to examine: (i) the nature of the dopaminergic adaptive mechanisms that come into action; (ii) their sequential activation in relation to the severity of degeneration; and (iii) their efficacy with regard to the maintenance of a normal level of basal ganglia activity, we analysed the brains of mice treated daily with 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine (MPTP, 4 mg/kg, i.p.) and killed at 5-day intervals from day 0 (D0) to D20. Our results demonstrate the sequential activation of two compensatory mechanisms: (i) an increase in striatal tyrosine hydroxylase (TH) protein content attested by the persistence of TH immunolabelling up to D15, contrasting with the decrease observed in both the number of nigral TH-immunoreactive neurons (-70.2%) and striatal dopamine content (-38.4%); (ii) a downregulation of DA uptake in surviving terminals at D20 (73.4% of nigral degeneration). At this point, the failure of adaptive mechanisms to maintain striatal dopaminergic homeostasis is also illustrated by an increase in the cytochrome oxidase activity of substantia nigra pars reticulata, a marker of neuronal function. It has been postulated that an increase in dopamine release per pulse could constitute an adaptive mechanism. The data we present from our MPTP mice model infirm this hypothesis. This study explores the link between the degree of nigral degeneration and the sequential activation of dopaminergic compensatory mechanisms in the nigrostriatal pathway and, in so doing, proposes a rethink of the paradigm applied to these mechanisms.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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