Compensatory mechanisms in experimental and human parkinsonism: towards a dynamic approach.
Identifieur interne : 001425 ( PubMed/Curation ); précédent : 001424; suivant : 001426Compensatory mechanisms in experimental and human parkinsonism: towards a dynamic approach.
Auteurs : E. Bezard [France] ; C E GrossSource :
- Progress in neurobiology [ 0301-0082 ] ; 1998.
English descriptors
- KwdEn :
- MESH :
- chemical , physiology : Dopamine.
- physiology : Adaptation, Physiological, Nerve Regeneration, Neuronal Plasticity, Synaptic Transmission.
- physiopathology : Parkinson Disease.
- Animals, Humans, Models, Neurological.
Abstract
This paper provides an overview of the compensatory mechanisms which come into action during experimental and human parkinsonism. The intrinsic properties of the dopaminergic neurones of the substantia nigra pars compacta (SNc) which degenerate during Parkinson's disease are described in detail. It is generally considered that the nigrostriatal pathway is principally responsible for the compensatory preservation of dopaminergic function. It is also becoming clear that the morphological characteristics of dopaminergic neurones and the dual character, synaptic and asynaptic, of striatal dopaminergic innervation engender two modes of transmission, wiring and volume, and that both these modes play a role in the preservation of dopaminergic function. The plasticity of the dopamine neurones, extrinsic or intrinsic to the striatum, can thus be regarded as another compensatory mechanism. Recent anatomical and electrophysiological studies have shown that the SNc receives both glutamatergic and cholinergic inputs. The dynamic role this innervation plays in compensatory mechanisms in the course of the disease is explained and discussed. Recent developments in the field of compensatory mechanisms speak for the urgence to develop a valid chronic model of Parkinson's disease, integrating all the clinical features, even resting tremor, and illustrating the gradual evolution of nigral degeneration observed in human Parkinson's disease. Only a dynamic approach to the physiopathological study of compensatory mechanisms in the basal ganglia will be capable of elucidating these complex questions.
PubMed: 9618745
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Bezard</name><affiliation wicri:level="1"><nlm:affiliation>Laboratoire de Neurophysiologie, CNRS UMR 5543, Université de Bordeaux II, France. erwan.bezard@umr5543.u-bordeaux2.fr</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Laboratoire de Neurophysiologie, CNRS UMR 5543, Université de Bordeaux II</wicri:regionArea></affiliation></author><author><name sortKey="Gross, C E" sort="Gross, C E" uniqKey="Gross C" first="C E" last="Gross">C E Gross</name></author></analytic><series><title level="j">Progress in neurobiology</title><idno type="ISSN">0301-0082</idno><imprint><date when="1998" type="published">1998</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptation, Physiological (physiology)</term><term>Animals</term><term>Dopamine (physiology)</term><term>Humans</term><term>Models, Neurological</term><term>Nerve Regeneration (physiology)</term><term>Neuronal Plasticity (physiology)</term><term>Parkinson Disease (physiopathology)</term><term>Synaptic Transmission (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Adaptation, Physiological</term><term>Nerve Regeneration</term><term>Neuronal Plasticity</term><term>Synaptic Transmission</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>Humans</term><term>Models, Neurological</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">This paper provides an overview of the compensatory mechanisms which come into action during experimental and human parkinsonism. The intrinsic properties of the dopaminergic neurones of the substantia nigra pars compacta (SNc) which degenerate during Parkinson's disease are described in detail. It is generally considered that the nigrostriatal pathway is principally responsible for the compensatory preservation of dopaminergic function. It is also becoming clear that the morphological characteristics of dopaminergic neurones and the dual character, synaptic and asynaptic, of striatal dopaminergic innervation engender two modes of transmission, wiring and volume, and that both these modes play a role in the preservation of dopaminergic function. The plasticity of the dopamine neurones, extrinsic or intrinsic to the striatum, can thus be regarded as another compensatory mechanism. Recent anatomical and electrophysiological studies have shown that the SNc receives both glutamatergic and cholinergic inputs. The dynamic role this innervation plays in compensatory mechanisms in the course of the disease is explained and discussed. Recent developments in the field of compensatory mechanisms speak for the urgence to develop a valid chronic model of Parkinson's disease, integrating all the clinical features, even resting tremor, and illustrating the gradual evolution of nigral degeneration observed in human Parkinson's disease. Only a dynamic approach to the physiopathological study of compensatory mechanisms in the basal ganglia will be capable of elucidating these complex questions.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9618745</PMID><DateCreated><Year>1998</Year><Month>08</Month><Day>20</Day></DateCreated><DateCompleted><Year>1998</Year><Month>08</Month><Day>20</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0301-0082</ISSN><JournalIssue CitedMedium="Print"><Volume>55</Volume><Issue>2</Issue><PubDate><Year>1998</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Progress in neurobiology</Title><ISOAbbreviation>Prog. Neurobiol.</ISOAbbreviation></Journal><ArticleTitle>Compensatory mechanisms in experimental and human parkinsonism: towards a dynamic approach.</ArticleTitle><Pagination><MedlinePgn>93-116</MedlinePgn></Pagination><Abstract><AbstractText>This paper provides an overview of the compensatory mechanisms which come into action during experimental and human parkinsonism. The intrinsic properties of the dopaminergic neurones of the substantia nigra pars compacta (SNc) which degenerate during Parkinson's disease are described in detail. It is generally considered that the nigrostriatal pathway is principally responsible for the compensatory preservation of dopaminergic function. It is also becoming clear that the morphological characteristics of dopaminergic neurones and the dual character, synaptic and asynaptic, of striatal dopaminergic innervation engender two modes of transmission, wiring and volume, and that both these modes play a role in the preservation of dopaminergic function. The plasticity of the dopamine neurones, extrinsic or intrinsic to the striatum, can thus be regarded as another compensatory mechanism. Recent anatomical and electrophysiological studies have shown that the SNc receives both glutamatergic and cholinergic inputs. The dynamic role this innervation plays in compensatory mechanisms in the course of the disease is explained and discussed. Recent developments in the field of compensatory mechanisms speak for the urgence to develop a valid chronic model of Parkinson's disease, integrating all the clinical features, even resting tremor, and illustrating the gradual evolution of nigral degeneration observed in human Parkinson's disease. 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