Preserved ipsilateral-to-lesion motor map organization in the unilateral 6-OHDA-treated rat model of Parkinson's disease
Identifieur interne : 000853 ( PascalFrancis/Checkpoint ); précédent : 000852; suivant : 000854Preserved ipsilateral-to-lesion motor map organization in the unilateral 6-OHDA-treated rat model of Parkinson's disease
Auteurs : Gerlinde A. Metz [Canada] ; Dionne M. Piecharka [Canada] ; Jeffrey A. Kleim [Canada] ; Ian Q. Whishaw [Canada]Source :
- Brain research [ 0006-8993 ] ; 2004.
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- Pascal (Inist)
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Abstract
The classic view of dopamine (DA) loss in Parkinson's disease is that it produces a functional deafferentation in striatal-cortical circuitry that, in turn, contributes to sensorimotor deficits. The present study examines this view in the rat by assessing how DA-depletion affects the intracortical microstimulation (ICMS) topographic representation of movement in the rostral and caudal motor areas of the motor cortex. The ICMS map is used as an index of motor cortex function because it has been shown to reflect motor function and experience. Groups of rats received no training or skilled reach training and were then given unilateral 6-hydroxydopamine (6-OHDA) or sham lesions of the nigrostriatal bundle to deplete nigrostriatal DA. Lesion success was confirmed by abnormalities in skilled reaching, by apomorphine-induced rotation, and by loss of DA neurons in the substantia nigra. The size and threshold of the motor map in naive and skilled reach trained DA-depleted rats were preserved. In addition, there was an increase in distal limb representation in the caudal forelimb area (CFA) in the DA-depleted rats suggesting a possible plastic response to the behavioral effects of DA-depletion. The presence of preserved size and modified map organization in DA-depleted rats is discussed in relation to the hypothesis that preserved motor cortex functionality despite DA loss underlies the spared motor abilities of DA-depleted rats.
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Metz</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Canadian Centre for Behavioural Neuroscience, University of Lethbridge</s1><s2>Lethbridge, AB, T1K 3M4</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Lethbridge, AB, T1K 3M4</wicri:noRegion></affiliation></author><author><name sortKey="Piecharka, Dionne M" sort="Piecharka, Dionne M" uniqKey="Piecharka D" first="Dionne M." last="Piecharka">Dionne M. Piecharka</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Canadian Centre for Behavioural Neuroscience, University of Lethbridge</s1><s2>Lethbridge, AB, T1K 3M4</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Lethbridge, AB, T1K 3M4</wicri:noRegion></affiliation></author><author><name sortKey="Kleim, Jeffrey A" sort="Kleim, Jeffrey A" uniqKey="Kleim J" first="Jeffrey A." last="Kleim">Jeffrey A. Kleim</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Canadian Centre for Behavioural Neuroscience, University of Lethbridge</s1><s2>Lethbridge, AB, T1K 3M4</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Lethbridge, AB, T1K 3M4</wicri:noRegion></affiliation></author><author><name sortKey="Whishaw, Ian Q" sort="Whishaw, Ian Q" uniqKey="Whishaw I" first="Ian Q." last="Whishaw">Ian Q. Whishaw</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Canadian Centre for Behavioural Neuroscience, University of Lethbridge</s1><s2>Lethbridge, AB, T1K 3M4</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Lethbridge, AB, T1K 3M4</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Brain research</title><title level="j" type="abbreviated">Brain res.</title><idno type="ISSN">0006-8993</idno><imprint><date when="2004">2004</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Brain research</title><title level="j" type="abbreviated">Brain res.</title><idno type="ISSN">0006-8993</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal model</term><term>Cerebral cortex</term><term>Lesion</term><term>Oxidopamine</term><term>Parkinson disease</term><term>Plasticity</term><term>Rat</term><term>Rotation</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Lésion</term><term>Oxidopamine</term><term>Modèle animal</term><term>Plasticité</term><term>Cortex cérébral</term><term>Rotation</term><term>Parkinson maladie</term><term>Rat</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The classic view of dopamine (DA) loss in Parkinson's disease is that it produces a functional deafferentation in striatal-cortical circuitry that, in turn, contributes to sensorimotor deficits. 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In addition, there was an increase in distal limb representation in the caudal forelimb area (CFA) in the DA-depleted rats suggesting a possible plastic response to the behavioral effects of DA-depletion. 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Metz</name></noRegion><name sortKey="Kleim, Jeffrey A" sort="Kleim, Jeffrey A" uniqKey="Kleim J" first="Jeffrey A." last="Kleim">Jeffrey A. Kleim</name><name sortKey="Piecharka, Dionne M" sort="Piecharka, Dionne M" uniqKey="Piecharka D" first="Dionne M." last="Piecharka">Dionne M. Piecharka</name><name sortKey="Whishaw, Ian Q" sort="Whishaw, Ian Q" uniqKey="Whishaw I" first="Ian Q." last="Whishaw">Ian Q. Whishaw</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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