Complex deficits on reaction time performance following bilateral intrastriatal 6-OHDA infusion in the rat.
Identifieur interne : 005005 ( Main/Merge ); précédent : 005004; suivant : 005006Complex deficits on reaction time performance following bilateral intrastriatal 6-OHDA infusion in the rat.
Auteurs : M. Amalric [France] ; H. Moukhles ; A. Nieoullon ; A. DaszutaSource :
- The European journal of neuroscience [ 0953-816X ] ; 1995.
English descriptors
- KwdEn :
- 3,4-Dihydroxyphenylacetic Acid (metabolism), Animals, Corpus Striatum (drug effects), Disease Models, Animal, Dopamine (metabolism), Frontal Lobe (pathology), Homovanillic Acid (metabolism), Immunohistochemistry, Male, Oxidopamine (pharmacology), Parkinson Disease (physiopathology), Rats, Rats, Wistar, Reaction Time (drug effects), Task Performance and Analysis.
- MESH :
- chemical , metabolism : 3,4-Dihydroxyphenylacetic Acid, Dopamine, Homovanillic Acid.
- drug effects : Corpus Striatum, Reaction Time.
- pathology : Frontal Lobe.
- chemical , pharmacology : Oxidopamine.
- physiopathology : Parkinson Disease.
- Animals, Disease Models, Animal, Immunohistochemistry, Male, Rats, Rats, Wistar, Task Performance and Analysis.
Abstract
The present study examined the ability of rats subjected to bilateral 6-hydroxydopamine lesions of the terminal area of the nigrostriatal dopamine system to perform a prelearned reaction time task. This lesion model, the induction of a partial dopamine denervation of the striatum (74% depletion of dopamine striatal tissue content) with a retrograde degeneration of dopamine cell bodies in the substantia nigra, sparing the mesolimbic dopaminergic pathway, closely approximates the neuronal degeneration observed in human idiopathic Parkinson's disease. Rats were trained previously to release a lever, within a reaction time limit, after the presentation of a visual cue through reinforcement with food pellets. The onset of the light stimulus varied randomly after an unpredictable delay period of 0.25-1.0 s. Rats with dopaminergic lesions showed moderate to extensive performance deficits which were not compensated for the five postoperative weeks. More than half of the lesioned animals (64%) showed severe deficits, characterized by a concomitant increase in the number of anticipated (premature release of the lever before the visual cue) and delayed responses (lever release after the reaction time limit) with shortened reaction times in some cases. A smaller proportion (36%) of lesioned animals exhibited mild impairment of performance with a large increase in delayed responses and lengthening of reaction times but with no change in the number of anticipated responses. Asymmetric lesions had no effect on the reaction time performance. Examination of tyrosine hydroxylase immunostaining revealed that in the most impaired animals dopamine depletion was extensive in the medial striatum, whereas it was restricted to the dorsolateral striatum in the least impaired animals.(ABSTRACT TRUNCATED AT 250 WORDS)
PubMed: 7613632
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Amalric</name><affiliation wicri:level="3"><nlm:affiliation>Laboratoire de Neurobiologie Cellulaire et Fonctionnelle (Laboratoire associé à l'Université Aix-Marseille II), CNRS, Marseille, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Laboratoire de Neurobiologie Cellulaire et Fonctionnelle (Laboratoire associé à l'Université Aix-Marseille II), CNRS, Marseille</wicri:regionArea><placeName><region type="region">Provence-Alpes-Côte d'Azur</region><region type="old region">Provence-Alpes-Côte d'Azur</region><settlement type="city">Marseille</settlement></placeName></affiliation></author><author><name sortKey="Moukhles, H" sort="Moukhles, H" uniqKey="Moukhles H" first="H" last="Moukhles">H. Moukhles</name></author><author><name sortKey="Nieoullon, A" sort="Nieoullon, A" uniqKey="Nieoullon A" first="A" last="Nieoullon">A. Nieoullon</name></author><author><name sortKey="Daszuta, A" sort="Daszuta, A" uniqKey="Daszuta A" first="A" last="Daszuta">A. Daszuta</name></author></analytic><series><title level="j">The European journal of neuroscience</title><idno type="ISSN">0953-816X</idno><imprint><date when="1995" type="published">1995</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>Corpus Striatum (drug effects)</term><term>Disease Models, Animal</term><term>Dopamine (metabolism)</term><term>Frontal Lobe (pathology)</term><term>Homovanillic Acid (metabolism)</term><term>Immunohistochemistry</term><term>Male</term><term>Oxidopamine (pharmacology)</term><term>Parkinson Disease (physiopathology)</term><term>Rats</term><term>Rats, Wistar</term><term>Reaction Time (drug effects)</term><term>Task Performance and Analysis</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>3,4-Dihydroxyphenylacetic Acid</term><term>Dopamine</term><term>Homovanillic Acid</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Corpus Striatum</term><term>Reaction Time</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Frontal Lobe</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Oxidopamine</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Immunohistochemistry</term><term>Male</term><term>Rats</term><term>Rats, Wistar</term><term>Task Performance and Analysis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The present study examined the ability of rats subjected to bilateral 6-hydroxydopamine lesions of the terminal area of the nigrostriatal dopamine system to perform a prelearned reaction time task. This lesion model, the induction of a partial dopamine denervation of the striatum (74% depletion of dopamine striatal tissue content) with a retrograde degeneration of dopamine cell bodies in the substantia nigra, sparing the mesolimbic dopaminergic pathway, closely approximates the neuronal degeneration observed in human idiopathic Parkinson's disease. Rats were trained previously to release a lever, within a reaction time limit, after the presentation of a visual cue through reinforcement with food pellets. The onset of the light stimulus varied randomly after an unpredictable delay period of 0.25-1.0 s. Rats with dopaminergic lesions showed moderate to extensive performance deficits which were not compensated for the five postoperative weeks. More than half of the lesioned animals (64%) showed severe deficits, characterized by a concomitant increase in the number of anticipated (premature release of the lever before the visual cue) and delayed responses (lever release after the reaction time limit) with shortened reaction times in some cases. A smaller proportion (36%) of lesioned animals exhibited mild impairment of performance with a large increase in delayed responses and lengthening of reaction times but with no change in the number of anticipated responses. Asymmetric lesions had no effect on the reaction time performance. Examination of tyrosine hydroxylase immunostaining revealed that in the most impaired animals dopamine depletion was extensive in the medial striatum, whereas it was restricted to the dorsolateral striatum in the least impaired animals.(ABSTRACT TRUNCATED AT 250 WORDS)</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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