Functional reinnervation from remaining DA terminals induced by GDNF lentivirus in a rat model of early Parkinson's disease.
Identifieur interne : 000D80 ( PubMed/Checkpoint ); précédent : 000D79; suivant : 000D81Functional reinnervation from remaining DA terminals induced by GDNF lentivirus in a rat model of early Parkinson's disease.
Auteurs : Mara Brizard [France] ; Carole Carcenac ; Alexis-Pierre Bemelmans ; Claude Feuerstein ; Jacques Mallet ; Marc SavastaSource :
- Neurobiology of disease [ 0969-9961 ] ; 2006.
English descriptors
- KwdEn :
- Animals, Corpus Striatum (physiopathology), Disease Models, Animal, Dopamine (physiology), Genetic Therapy (methods), Glial Cell Line-Derived Neurotrophic Factor (genetics), Lentivirus (genetics), Male, Movement, Nerve Degeneration (physiopathology), Nerve Degeneration (therapy), Nerve Regeneration, Oxidopamine (toxicity), Parkinson Disease (physiopathology), Parkinson Disease (therapy), Presynaptic Terminals (physiology), Rats, Rats, Sprague-Dawley, Recovery of Function, Sympatholytics (toxicity).
- MESH :
- chemical , genetics : Glial Cell Line-Derived Neurotrophic Factor.
- chemical , physiology : Dopamine.
- genetics : Lentivirus.
- methods : Genetic Therapy.
- physiology : Presynaptic Terminals.
- physiopathology : Corpus Striatum, Nerve Degeneration, Parkinson Disease.
- therapy : Nerve Degeneration, Parkinson Disease.
- chemical , toxicity : Oxidopamine, Sympatholytics.
- Animals, Disease Models, Animal, Male, Movement, Nerve Regeneration, Rats, Rats, Sprague-Dawley, Recovery of Function.
Abstract
Glial cell-line derived neurotrophic factor (GDNF) is a good candidate agent for restoring functional reinnervation and/or neuroprotection of dopamine (DA) nigrostriatal system and thus for the treatment of Parkinson's disease (PD). Viral delivery is currently the most likely in vivo strategy for delivery of the therapeutic protein into the brain for treatment of neurological diseases. However, one of the important unresolved issues for this strategy is the threshold number of DA nigral neurons and/or of striatal DA terminals necessary for optimal benefit from GDNF therapy. In this study, we examined the intrastriatal neurotrophic effects of long-term GDNF delivery using a lentiviral vector in a new rat model of early PD. Lenti-GDNF was injected into the striatum 4 weeks after partial substantia nigra pars compacta 6-hydroxydopamine-induced lesion. Striatal denervation was evaluated by assessing tyrosine hydroxylase-positive DA fiber density and corroborated by testing motor deficit by means of a staircase test. GDNF treatment restored complete striatal DA innervation in the previously denervated area and this was associated with significant behavioral improvements.
DOI: 10.1016/j.nbd.2005.06.015
PubMed: 16084732
Affiliations:
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pubmed:16084732Le document en format XML
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(physiopathology)</term><term>Parkinson Disease (therapy)</term><term>Presynaptic Terminals (physiology)</term><term>Rats</term><term>Rats, Sprague-Dawley</term><term>Recovery of Function</term><term>Sympatholytics (toxicity)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Glial Cell Line-Derived Neurotrophic Factor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Lentivirus</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Genetic Therapy</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Presynaptic Terminals</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Corpus Striatum</term><term>Nerve Degeneration</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="therapy" 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Viral delivery is currently the most likely in vivo strategy for delivery of the therapeutic protein into the brain for treatment of neurological diseases. However, one of the important unresolved issues for this strategy is the threshold number of DA nigral neurons and/or of striatal DA terminals necessary for optimal benefit from GDNF therapy. In this study, we examined the intrastriatal neurotrophic effects of long-term GDNF delivery using a lentiviral vector in a new rat model of early PD. Lenti-GDNF was injected into the striatum 4 weeks after partial substantia nigra pars compacta 6-hydroxydopamine-induced lesion. Striatal denervation was evaluated by assessing tyrosine hydroxylase-positive DA fiber density and corroborated by testing motor deficit by means of a staircase test. GDNF treatment restored complete striatal DA innervation in the previously denervated area and this was associated with significant behavioral improvements.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16084732</PMID><DateCreated><Year>2005</Year><Month>12</Month><Day>26</Day></DateCreated><DateCompleted><Year>2006</Year><Month>03</Month><Day>09</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0969-9961</ISSN><JournalIssue CitedMedium="Print"><Volume>21</Volume><Issue>1</Issue><PubDate><Year>2006</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Neurobiology of disease</Title><ISOAbbreviation>Neurobiol. 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Lenti-GDNF was injected into the striatum 4 weeks after partial substantia nigra pars compacta 6-hydroxydopamine-induced lesion. Striatal denervation was evaluated by assessing tyrosine hydroxylase-positive DA fiber density and corroborated by testing motor deficit by means of a staircase test. GDNF treatment restored complete striatal DA innervation in the previously denervated area and this was associated with significant behavioral improvements.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Brizard</LastName><ForeName>Mara</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Laboratoire de Génétique Moléculaire des Processus Neurodégénératifs et de la Neurotransmission-Unité Mixte de Recherche, bâtiment CERVI, 83 boulevard de l'Hôpital, 75013 PARIS, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Carcenac</LastName><ForeName>Carole</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Bemelmans</LastName><ForeName>Alexis-Pierre</ForeName><Initials>AP</Initials></Author><Author ValidYN="Y"><LastName>Feuerstein</LastName><ForeName>Claude</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Mallet</LastName><ForeName>Jacques</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Savasta</LastName><ForeName>Marc</ForeName><Initials>M</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2005</Year><Month>08</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neurobiol Dis</MedlineTA><NlmUniqueID>9500169</NlmUniqueID><ISSNLinking>0969-9961</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051100">Glial Cell Line-Derived Neurotrophic Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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UI="D013565" MajorTopicYN="N">Sympatholytics</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2005</Year><Month>02</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2005</Year><Month>06</Month><Day>03</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2005</Year><Month>06</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>8</Month><Day>9</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>3</Month><Day>10</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2005</Year><Month>8</Month><Day>9</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16084732</ArticleId><ArticleId IdType="pii">S0969-9961(05)00191-9</ArticleId><ArticleId IdType="doi">10.1016/j.nbd.2005.06.015</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Île-de-France</li></region><settlement><li>PARIS</li></settlement></list><tree><noCountry><name sortKey="Bemelmans, Alexis Pierre" sort="Bemelmans, Alexis Pierre" uniqKey="Bemelmans A" first="Alexis-Pierre" last="Bemelmans">Alexis-Pierre Bemelmans</name><name sortKey="Carcenac, Carole" sort="Carcenac, Carole" uniqKey="Carcenac C" first="Carole" last="Carcenac">Carole Carcenac</name><name sortKey="Feuerstein, Claude" sort="Feuerstein, Claude" uniqKey="Feuerstein C" first="Claude" last="Feuerstein">Claude Feuerstein</name><name sortKey="Mallet, Jacques" sort="Mallet, Jacques" uniqKey="Mallet J" first="Jacques" last="Mallet">Jacques Mallet</name><name sortKey="Savasta, Marc" sort="Savasta, Marc" uniqKey="Savasta M" first="Marc" last="Savasta">Marc Savasta</name></noCountry><country name="France"><region name="Île-de-France"><name sortKey="Brizard, Mara" sort="Brizard, Mara" uniqKey="Brizard M" first="Mara" last="Brizard">Mara Brizard</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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