Preserved ipsilateral-to-lesion motor map organization in the unilateral 6-OHDA-treated rat model of Parkinson's disease.
Identifieur interne : 002F13 ( Main/Merge ); précédent : 002F12; suivant : 002F14Preserved 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 ; Jeffrey A. Kleim ; Ian Q. WhishawSource :
- Brain research [ 0006-8993 ] ; 2004.
English descriptors
- KwdEn :
- Analysis of Variance, Animals, Apomorphine (pharmacology), Behavior, Animal, Brain (physiopathology), Brain (radiation effects), Brain Mapping, Cell Count, Disease Models, Animal, Dopamine (deficiency), Electric Stimulation (methods), Forelimb (innervation), Forelimb (physiopathology), Functional Laterality (physiology), Immunohistochemistry (methods), Male, Movement (drug effects), Movement (physiology), Oxidopamine, Parkinson Disease (etiology), Parkinson Disease (metabolism), Parkinson Disease (physiopathology), Psychomotor Performance (physiology), Rats, Rats, Long-Evans, Rotation, Sympatholytics, Tyrosine 3-Monooxygenase (metabolism).
- MESH :
- chemical , deficiency : Dopamine.
- chemical , metabolism : Tyrosine 3-Monooxygenase.
- chemical , pharmacology : Apomorphine.
- drug effects : Movement.
- etiology : Parkinson Disease.
- innervation : Forelimb.
- metabolism : Parkinson Disease.
- methods : Electric Stimulation, Immunohistochemistry.
- physiology : Functional Laterality, Movement, Psychomotor Performance.
- physiopathology : Brain, Forelimb, Parkinson Disease.
- radiation effects : Brain.
- Analysis of Variance, Animals, Behavior, Animal, Brain Mapping, Cell Count, Disease Models, Animal, Male, Oxidopamine, Rats, Rats, Long-Evans, Rotation, Sympatholytics.
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.
DOI: 10.1016/j.brainres.2004.08.025
PubMed: 15476704
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Metz</name><affiliation wicri:level="1"><nlm:affiliation>Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, Canada, T1K 3M4, Canada gerlinde.metz@uleth.ca.</nlm:affiliation><country wicri:rule="url">Canada</country><wicri:regionArea>Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, Canada, T1K 3M4</wicri:regionArea><wicri:noRegion>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></author><author><name sortKey="Kleim, Jeffrey A" sort="Kleim, Jeffrey A" uniqKey="Kleim J" first="Jeffrey A" last="Kleim">Jeffrey A. Kleim</name></author><author><name sortKey="Whishaw, Ian Q" sort="Whishaw, Ian Q" uniqKey="Whishaw I" first="Ian Q" last="Whishaw">Ian Q. Whishaw</name></author></analytic><series><title level="j">Brain research</title><idno type="ISSN">0006-8993</idno><imprint><date when="2004" type="published">2004</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Analysis of Variance</term><term>Animals</term><term>Apomorphine (pharmacology)</term><term>Behavior, Animal</term><term>Brain (physiopathology)</term><term>Brain (radiation effects)</term><term>Brain Mapping</term><term>Cell Count</term><term>Disease Models, Animal</term><term>Dopamine (deficiency)</term><term>Electric Stimulation (methods)</term><term>Forelimb (innervation)</term><term>Forelimb (physiopathology)</term><term>Functional Laterality (physiology)</term><term>Immunohistochemistry (methods)</term><term>Male</term><term>Movement (drug effects)</term><term>Movement (physiology)</term><term>Oxidopamine</term><term>Parkinson Disease (etiology)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (physiopathology)</term><term>Psychomotor Performance (physiology)</term><term>Rats</term><term>Rats, Long-Evans</term><term>Rotation</term><term>Sympatholytics</term><term>Tyrosine 3-Monooxygenase (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Tyrosine 3-Monooxygenase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Apomorphine</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Movement</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="innervation" xml:lang="en"><term>Forelimb</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Electric Stimulation</term><term>Immunohistochemistry</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Functional Laterality</term><term>Movement</term><term>Psychomotor Performance</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Brain</term><term>Forelimb</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="radiation effects" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Analysis of Variance</term><term>Animals</term><term>Behavior, Animal</term><term>Brain Mapping</term><term>Cell Count</term><term>Disease Models, Animal</term><term>Male</term><term>Oxidopamine</term><term>Rats</term><term>Rats, Long-Evans</term><term>Rotation</term><term>Sympatholytics</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. 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.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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