La maladie de Parkinson au Canada (serveur d'exploration)

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Preserved ipsilateral-to-lesion motor map organization in the unilateral 6-OHDA-treated rat model of Parkinson's disease

Identifieur interne : 000950 ( PascalFrancis/Corpus ); précédent : 000949; suivant : 000951

Preserved ipsilateral-to-lesion motor map organization in the unilateral 6-OHDA-treated rat model of Parkinson's disease

Auteurs : Gerlinde A. Metz ; Dionne M. Piecharka ; Jeffrey A. Kleim ; Ian Q. Whishaw

Source :

RBID : Pascal:04-0586177

Descripteurs français

English descriptors

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.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A08 01  1  ENG  @1 Preserved ipsilateral-to-lesion motor map organization in the unilateral 6-OHDA-treated rat model of Parkinson's disease
A11 01  1    @1 METZ (Gerlinde A.)
A11 02  1    @1 PIECHARKA (Dionne M.)
A11 03  1    @1 KLEIM (Jeffrey A.)
A11 04  1    @1 WHISHAW (Ian Q.)
A14 01      @1 Canadian Centre for Behavioural Neuroscience, University of Lethbridge @2 Lethbridge, AB, T1K 3M4 @3 CAN @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut.
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C01 01    ENG  @0 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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Format Inist (serveur)

NO : PASCAL 04-0586177 INIST
ET : Preserved ipsilateral-to-lesion motor map organization in the unilateral 6-OHDA-treated rat model of Parkinson's disease
AU : METZ (Gerlinde A.); PIECHARKA (Dionne M.); KLEIM (Jeffrey A.); WHISHAW (Ian Q.)
AF : Canadian Centre for Behavioural Neuroscience, University of Lethbridge/Lethbridge, AB, T1K 3M4/Canada (1 aut., 2 aut., 3 aut., 4 aut.)
DT : Publication en série; Niveau analytique
SO : Brain research; ISSN 0006-8993; Coden BRREAP; Pays-Bas; Da. 2004; Vol. 1026; No. 1; Pp. 126-135; Bibl. 82 ref.
LA : Anglais
EA : 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.
CC : 002B17G
FD : Lésion; Oxidopamine; Modèle animal; Plasticité; Cortex cérébral; Rotation; Parkinson maladie; Rat
FG : Encéphale; Système nerveux central; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Rodentia; Mammalia; Vertebrata
ED : Lesion; Oxidopamine; Animal model; Plasticity; Cerebral cortex; Rotation; Parkinson disease; Rat
EG : Encephalon; Central nervous system; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Rodentia; Mammalia; Vertebrata
SD : Lesión; Oxidopamina; Modelo animal; Plasticidad; Corteza cerebral; Rotación; Parkinson enfermedad; Rata
LO : INIST-12895.354000114269550130
ID : 04-0586177

Links to Exploration step

Pascal:04-0586177

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<s5>06</s5>
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<s5>54</s5>
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<s5>32</s5>
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<s5>32</s5>
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<s5>39</s5>
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<s5>39</s5>
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<s5>40</s5>
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<s5>41</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>41</s5>
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<fC07 i1="06" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>42</s5>
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<fC07 i1="07" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>42</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>42</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE">
<s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="ENG">
<s0>Rodentia</s0>
<s2>NS</s2>
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<fC07 i1="08" i2="X" l="SPA">
<s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="09" i2="X" l="FRE">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="09" i2="X" l="ENG">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="09" i2="X" l="SPA">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="10" i2="X" l="FRE">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="10" i2="X" l="ENG">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="10" i2="X" l="SPA">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fN21>
<s1>334</s1>
</fN21>
</pA>
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<server>
<NO>PASCAL 04-0586177 INIST</NO>
<ET>Preserved ipsilateral-to-lesion motor map organization in the unilateral 6-OHDA-treated rat model of Parkinson's disease</ET>
<AU>METZ (Gerlinde A.); PIECHARKA (Dionne M.); KLEIM (Jeffrey A.); WHISHAW (Ian Q.)</AU>
<AF>Canadian Centre for Behavioural Neuroscience, University of Lethbridge/Lethbridge, AB, T1K 3M4/Canada (1 aut., 2 aut., 3 aut., 4 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Brain research; ISSN 0006-8993; Coden BRREAP; Pays-Bas; Da. 2004; Vol. 1026; No. 1; Pp. 126-135; Bibl. 82 ref.</SO>
<LA>Anglais</LA>
<EA>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.</EA>
<CC>002B17G</CC>
<FD>Lésion; Oxidopamine; Modèle animal; Plasticité; Cortex cérébral; Rotation; Parkinson maladie; Rat</FD>
<FG>Encéphale; Système nerveux central; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Rodentia; Mammalia; Vertebrata</FG>
<ED>Lesion; Oxidopamine; Animal model; Plasticity; Cerebral cortex; Rotation; Parkinson disease; Rat</ED>
<EG>Encephalon; Central nervous system; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Rodentia; Mammalia; Vertebrata</EG>
<SD>Lesión; Oxidopamina; Modelo animal; Plasticidad; Corteza cerebral; Rotación; Parkinson enfermedad; Rata</SD>
<LO>INIST-12895.354000114269550130</LO>
<ID>04-0586177</ID>
</server>
</inist>
</record>

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