Striatal synaptic plasticity: Implications for motor learning and Parkinson's disease
Identifieur interne : 003719 ( Main/Exploration ); précédent : 003718; suivant : 003720Striatal synaptic plasticity: Implications for motor learning and Parkinson's disease
Auteurs : Antonio Pisani [Italie] ; Diego Centonze [Italie] ; Giorgio Bernardi [Italie] ; Paolo Calabresi [Italie]Source :
- Movement Disorders [ 0885-3185 ] ; 2005-04.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Animals, Antiparkinson Agents (adverse effects), Corpus Striatum (pathology), Corpus Striatum (physiopathology), Disease Models, Animal, Dopamine, Dyskinesia, Dyskinesia, Drug-Induced (etiology), Humans, Learning, Levodopa, Levodopa (adverse effects), Motor Skills (physiology), Motor learning, Nervous system diseases, Neural Pathways (physiopathology), Neuronal Plasticity (physiology), Parkinson Disease (drug therapy), Parkinson Disease (pathology), Parkinson Disease (physiopathology), Parkinson disease, Parkinson's disease, Rats, Synapses (pathology), Synaptic plasticity, dopamine, 6‐hydroxydopamine, levodopa‐induced dyskinesias, striatum, synaptic plasticity.
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- drug therapy : Parkinson Disease.
- etiology : Dyskinesia, Drug-Induced.
- pathology : Corpus Striatum, Parkinson Disease, Synapses.
- physiology : Motor Skills, Neuronal Plasticity.
- physiopathology : Corpus Striatum, Neural Pathways, Parkinson Disease.
- Animals, Disease Models, Animal, Humans, Learning, Rats.
Abstract
Changing the strength of synaptic connections between neurons is widely assumed to be the mechanism by which memory traces are encoded and stored in the central nervous system. Plastic changes appear to follow a regional specialization and underlie the specific type of memory mediated by the brain area in which plasticity occurs. Thus, long‐term changes occurring at excitatory corticostriatal synapses should be critically involved in motor learning. Indeed, repetitive stimulation of the corticostriatal pathway can cause either a long‐lasting increase or an enduring decrease in synaptic strength, respectively referred to as long‐term potentiation (LTP), and long‐term depression, both requiring a complex sequence of biochemical events. Once established, LTP can be reversed to control levels by a low‐frequency stimulation protocol, an active phenomenon defined “synaptic depotentiation,” required to erase redundant information. In the 6‐hydroxydopamine rat model of Parkinson's disease (PD), striatal synaptic plasticity has been shown to be impaired, although chronic treatment with levodopa was able to restore it. Of interest, a consistent number of L‐dopa–treated animals developed involuntary movements, resembling human dyskinesias. Strikingly, electrophysiological recordings from the dyskinetic group of rats demonstrated a selective impairment of synaptic depotentiation. This survey will provide an overview of plastic changes occurring at striatal synapses. The potential relevance of these findings in the control of motor function and in the pathogenesis both of PD and L‐dopa–induced motor complications will be discussed. © 2005 Movement Disorder Society
Url:
DOI: 10.1002/mds.20394
Affiliations:
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Le document en format XML
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2005-04">2005-04</date><biblScope unit="vol">20</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="395">395</biblScope><biblScope unit="page" to="402">402</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">BD72840F0593238211AE0C1377E0BBAA4C497EDA</idno><idno type="DOI">10.1002/mds.20394</idno><idno type="ArticleID">MDS20394</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antiparkinson Agents (adverse effects)</term><term>Corpus Striatum (pathology)</term><term>Corpus Striatum (physiopathology)</term><term>Disease Models, Animal</term><term>Dopamine</term><term>Dyskinesia</term><term>Dyskinesia, Drug-Induced (etiology)</term><term>Humans</term><term>Learning</term><term>Levodopa</term><term>Levodopa (adverse effects)</term><term>Motor Skills (physiology)</term><term>Motor learning</term><term>Nervous system diseases</term><term>Neural Pathways (physiopathology)</term><term>Neuronal Plasticity (physiology)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Rats</term><term>Synapses (pathology)</term><term>Synaptic plasticity</term><term>dopamine, 6‐hydroxydopamine</term><term>levodopa‐induced dyskinesias</term><term>striatum</term><term>synaptic plasticity</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Dyskinesia, Drug-Induced</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Corpus Striatum</term><term>Parkinson Disease</term><term>Synapses</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Motor Skills</term><term>Neuronal Plasticity</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Corpus Striatum</term><term>Neural Pathways</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Humans</term><term>Learning</term><term>Rats</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Apprentissage moteur</term><term>Dopamine</term><term>Dyskinésie</term><term>Lévodopa</term><term>Parkinson maladie</term><term>Plasticité synaptique</term><term>Système nerveux pathologie</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Changing the strength of synaptic connections between neurons is widely assumed to be the mechanism by which memory traces are encoded and stored in the central nervous system. Plastic changes appear to follow a regional specialization and underlie the specific type of memory mediated by the brain area in which plasticity occurs. Thus, long‐term changes occurring at excitatory corticostriatal synapses should be critically involved in motor learning. Indeed, repetitive stimulation of the corticostriatal pathway can cause either a long‐lasting increase or an enduring decrease in synaptic strength, respectively referred to as long‐term potentiation (LTP), and long‐term depression, both requiring a complex sequence of biochemical events. Once established, LTP can be reversed to control levels by a low‐frequency stimulation protocol, an active phenomenon defined “synaptic depotentiation,” required to erase redundant information. In the 6‐hydroxydopamine rat model of Parkinson's disease (PD), striatal synaptic plasticity has been shown to be impaired, although chronic treatment with levodopa was able to restore it. Of interest, a consistent number of L‐dopa–treated animals developed involuntary movements, resembling human dyskinesias. Strikingly, electrophysiological recordings from the dyskinetic group of rats demonstrated a selective impairment of synaptic depotentiation. This survey will provide an overview of plastic changes occurring at striatal synapses. The potential relevance of these findings in the control of motor function and in the pathogenesis both of PD and L‐dopa–induced motor complications will be discussed. © 2005 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Italie</li></country><region><li>Latium</li></region><settlement><li>Rome</li></settlement></list><tree><country name="Italie"><region name="Latium"><name sortKey="Pisani, Antonio" sort="Pisani, Antonio" uniqKey="Pisani A" first="Antonio" last="Pisani">Antonio Pisani</name></region><name sortKey="Bernardi, Giorgio" sort="Bernardi, Giorgio" uniqKey="Bernardi G" first="Giorgio" last="Bernardi">Giorgio Bernardi</name><name sortKey="Calabresi, Paolo" sort="Calabresi, Paolo" uniqKey="Calabresi P" first="Paolo" last="Calabresi">Paolo Calabresi</name><name sortKey="Centonze, Diego" sort="Centonze, Diego" uniqKey="Centonze D" first="Diego" last="Centonze">Diego Centonze</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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