A golgi analysis of cortical pyramidal cells in the unilateral parkinson rat: absence of change in the affected hemisphere vs hypertrophy in the intact hemisphere.
Identifieur interne : 002491 ( Main/Exploration ); précédent : 002490; suivant : 002492A golgi analysis of cortical pyramidal cells in the unilateral parkinson rat: absence of change in the affected hemisphere vs hypertrophy in the intact hemisphere.
Auteurs : Elena I. Miklyaeva [Canada] ; Ian Q. Whishaw ; Bryan KolbSource :
- Restorative neurology and neuroscience [ 0922-6028 ] ; 2007.
English descriptors
- KwdEn :
- Animals, Apomorphine (pharmacology), Cerebral Cortex (pathology), Dendrites (ultrastructure), Dendritic Spines (ultrastructure), Dextroamphetamine (pharmacology), Female, Forelimb (physiopathology), Golgi Apparatus (ultrastructure), Hypertrophy, Motor Activity (drug effects), Motor Cortex (pathology), Oxidopamine, Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (pathology), Parkinson Disease, Secondary (physiopathology), Psychomotor Performance, Pyramidal Cells (ultrastructure), Rats, Rats, Long-Evans, Rotation, Synapses (ultrastructure).
- MESH :
- chemical , pharmacology : Apomorphine, Dextroamphetamine.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Motor Activity.
- pathology : Cerebral Cortex, Motor Cortex, Parkinson Disease, Secondary.
- physiopathology : Forelimb, Parkinson Disease, Secondary.
- ultrastructure : Dendrites, Dendritic Spines, Golgi Apparatus, Pyramidal Cells, Synapses.
- Animals, Female, Hypertrophy, Oxidopamine, Psychomotor Performance, Rats, Rats, Long-Evans, Rotation.
Abstract
Unilateral dopamine (DA) depletion in the rat provides an analog of human Parkinson's disease. The classic view of DA loss is that it produces changes in the activity of striatal-cortical circuitry that results in reduced frontal cortex neural activity. This "functional deafferent" view is consistent with findings that animals display sensorimotor deficits in the contralateral-to-lesion side of the body and compensatory behavior adjustments in the ipsilateral-to-lesion side of the body. The present study examined how DA depletion and the associated sensorimotor changes affect the morphology of the ipsilateral or contralateral neocortex neurons as assessed by dendritic morphology in Golgi-stained tissue.
PubMed: 17726267
Affiliations:
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Le document en format XML
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Whishaw</name></author><author><name sortKey="Kolb, Bryan" sort="Kolb, Bryan" uniqKey="Kolb B" first="Bryan" last="Kolb">Bryan Kolb</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2007">2007</date><idno type="RBID">pubmed:17726267</idno><idno type="pmid">17726267</idno><idno type="wicri:Area/PubMed/Corpus">001119</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001119</idno><idno type="wicri:Area/PubMed/Curation">001119</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001119</idno><idno type="wicri:Area/PubMed/Checkpoint">001119</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001119</idno><idno type="wicri:Area/Ncbi/Merge">000806</idno><idno type="wicri:Area/Ncbi/Curation">000806</idno><idno type="wicri:Area/Ncbi/Checkpoint">000806</idno><idno type="wicri:doubleKey">0922-6028:2007:Miklyaeva E:a:golgi:analysis</idno><idno type="wicri:Area/Main/Merge">002734</idno><idno type="wicri:Area/Main/Curation">002491</idno><idno type="wicri:Area/Main/Exploration">002491</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">A golgi analysis of cortical pyramidal cells in the unilateral parkinson rat: absence of change in the affected hemisphere vs hypertrophy in the intact hemisphere.</title><author><name sortKey="Miklyaeva, Elena I" sort="Miklyaeva, Elena I" uniqKey="Miklyaeva E" first="Elena I" last="Miklyaeva">Elena I. Miklyaeva</name><affiliation wicri:level="1"><nlm:affiliation>Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, T1K 3M4, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, AB, T1K 3M4</wicri:regionArea><wicri:noRegion>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></author><author><name sortKey="Kolb, Bryan" sort="Kolb, Bryan" uniqKey="Kolb B" first="Bryan" last="Kolb">Bryan Kolb</name></author></analytic><series><title level="j">Restorative neurology and neuroscience</title><idno type="ISSN">0922-6028</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Apomorphine (pharmacology)</term><term>Cerebral Cortex (pathology)</term><term>Dendrites (ultrastructure)</term><term>Dendritic Spines (ultrastructure)</term><term>Dextroamphetamine (pharmacology)</term><term>Female</term><term>Forelimb (physiopathology)</term><term>Golgi Apparatus (ultrastructure)</term><term>Hypertrophy</term><term>Motor Activity (drug effects)</term><term>Motor Cortex (pathology)</term><term>Oxidopamine</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (pathology)</term><term>Parkinson Disease, Secondary (physiopathology)</term><term>Psychomotor Performance</term><term>Pyramidal Cells (ultrastructure)</term><term>Rats</term><term>Rats, Long-Evans</term><term>Rotation</term><term>Synapses (ultrastructure)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Apomorphine</term><term>Dextroamphetamine</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Motor Activity</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Cerebral Cortex</term><term>Motor Cortex</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Forelimb</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Dendrites</term><term>Dendritic Spines</term><term>Golgi Apparatus</term><term>Pyramidal Cells</term><term>Synapses</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Female</term><term>Hypertrophy</term><term>Oxidopamine</term><term>Psychomotor Performance</term><term>Rats</term><term>Rats, Long-Evans</term><term>Rotation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Unilateral dopamine (DA) depletion in the rat provides an analog of human Parkinson's disease. The classic view of DA loss is that it produces changes in the activity of striatal-cortical circuitry that results in reduced frontal cortex neural activity. This "functional deafferent" view is consistent with findings that animals display sensorimotor deficits in the contralateral-to-lesion side of the body and compensatory behavior adjustments in the ipsilateral-to-lesion side of the body. The present study examined how DA depletion and the associated sensorimotor changes affect the morphology of the ipsilateral or contralateral neocortex neurons as assessed by dendritic morphology in Golgi-stained tissue.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Kolb, Bryan" sort="Kolb, Bryan" uniqKey="Kolb B" first="Bryan" last="Kolb">Bryan Kolb</name><name sortKey="Whishaw, Ian Q" sort="Whishaw, Ian Q" uniqKey="Whishaw I" first="Ian Q" last="Whishaw">Ian Q. Whishaw</name></noCountry><country name="Canada"><noRegion><name sortKey="Miklyaeva, Elena I" sort="Miklyaeva, Elena I" uniqKey="Miklyaeva E" first="Elena I" last="Miklyaeva">Elena I. Miklyaeva</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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