Glial activation is associated with l-DOPA induced dyskinesia and blocked by a nitric oxide synthase inhibitor in a rat model of Parkinson's disease.
Identifieur interne : 000442 ( PubMed/Corpus ); précédent : 000441; suivant : 000443Glial activation is associated with l-DOPA induced dyskinesia and blocked by a nitric oxide synthase inhibitor in a rat model of Parkinson's disease.
Auteurs : Mariza Bortolanza ; Roberta Cavalcanti-Kiwiatkoski ; Fernando E. Padovan-Neto ; Célia Aparecida Da-Silva ; Miso Mitkovski ; Rita Raisman-Vozari ; Elaine Del-BelSource :
- Neurobiology of disease [ 1095-953X ] ; 2015.
English descriptors
- KwdEn :
- Animals, Antiparkinson Agents (adverse effects), Disease Models, Animal, Dyskinesia, Drug-Induced (drug therapy), Dyskinesia, Drug-Induced (metabolism), Indazoles (pharmacology), Inflammation (chemically induced), Levodopa (administration & dosage), Levodopa (adverse effects), Male, Neuroglia (metabolism), Neuroprotective Agents (pharmacology), Nitric Oxide (metabolism), Nitric Oxide Synthase (antagonists & inhibitors), Parkinson Disease (drug therapy), Rats, Rats, Wistar, Up-Regulation.
- MESH :
- chemical , administration & dosage : Levodopa.
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- chemical , antagonists & inhibitors : Nitric Oxide Synthase.
- chemically induced : Inflammation.
- drug therapy : Dyskinesia, Drug-Induced, Parkinson Disease.
- metabolism : Dyskinesia, Drug-Induced, Neuroglia, Nitric Oxide.
- chemical , pharmacology : Indazoles, Neuroprotective Agents.
- Animals, Disease Models, Animal, Male, Rats, Rats, Wistar, Up-Regulation.
Abstract
l-3, 4-dihydroxyphenylalanine (L-DOPA) is the most effective treatment for Parkinson's disease but can induce debilitating abnormal involuntary movements (dyskinesia). Here we show that the development of L-DOPA-induced dyskinesia in the rat is accompanied by upregulation of an inflammatory cascade involving nitric oxide. Male Wistar rats sustained unilateral injections of 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle. After three weeks animals started to receive daily treatment with L-DOPA (30 mg/kg plus benserazide 7.5 mg/kg, for 21 days), combined with an inhibitor of neuronal NOS (7-nitroindazole, 7-NI, 30 mg/kg/day) or vehicle (saline-PEG 50%). All animals treated with L-DOPA and vehicle developed abnormal involuntary movements, and this effect was prevented by 7-NI. L-DOPA-treated dyskinetic animals exhibited an increased striatal and pallidal expression of glial fibrillary acidic protein (GFAP) in reactive astrocytes, an increased number of CD11b-positive microglial cells with activated morphology, and the rise of cells positive for inducible nitric oxide-synthase immunoreactivity (iNOS). All these indexes of glial activation were prevented by 7-NI co-administration. These findings provide evidence that the development of L-DOPA-induced dyskinesia in the rat is associated with activation of glial cells that promote inflammatory responses. The dramatic effect of 7-NI in preventing this glial response points to an involvement of nitric oxide. Moreover, the results suggest that the NOS inhibitor prevents dyskinesia at least in part via inhibition of glial cell activation and iNOS expression. Our observations indicate nitric oxide synthase inhibitors as a therapeutic strategy for preventing neuroinflammatory and glial components of dyskinesia pathogenesis in Parkinson's disease.
DOI: 10.1016/j.nbd.2014.10.017
PubMed: 25447229
Links to Exploration step
pubmed:25447229Le document en format XML
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Café S/N, 14040-904 Ribeirão Preto, SP, Brazil; USP, Center for Interdisciplinary Research on Applied Neurosciences (NAPNA), Brazil.</nlm:affiliation></affiliation></author><author><name sortKey="Cavalcanti Kiwiatkoski, Roberta" sort="Cavalcanti Kiwiatkoski, Roberta" uniqKey="Cavalcanti Kiwiatkoski R" first="Roberta" last="Cavalcanti-Kiwiatkoski">Roberta Cavalcanti-Kiwiatkoski</name><affiliation><nlm:affiliation>USP, Center for Interdisciplinary Research on Applied Neurosciences (NAPNA), Brazil; USP, Medical School, Department of Physiology, Av. Bandeirantes 3900, 14049-900 Ribeirão Preto, SP, Brazil.</nlm:affiliation></affiliation></author><author><name sortKey="Padovan Neto, Fernando E" sort="Padovan Neto, Fernando E" uniqKey="Padovan Neto F" first="Fernando E" last="Padovan-Neto">Fernando E. Padovan-Neto</name><affiliation><nlm:affiliation>USP, Center for Interdisciplinary Research on Applied Neurosciences (NAPNA), Brazil; USP, Department of Behavioral Neurosciences, Av. 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Café S/N, 14040-904 Ribeirão Preto, SP, Brazil; USP, Center for Interdisciplinary Research on Applied Neurosciences (NAPNA), Brazil.</nlm:affiliation></affiliation></author><author><name sortKey="Cavalcanti Kiwiatkoski, Roberta" sort="Cavalcanti Kiwiatkoski, Roberta" uniqKey="Cavalcanti Kiwiatkoski R" first="Roberta" last="Cavalcanti-Kiwiatkoski">Roberta Cavalcanti-Kiwiatkoski</name><affiliation><nlm:affiliation>USP, Center for Interdisciplinary Research on Applied Neurosciences (NAPNA), Brazil; USP, Medical School, Department of Physiology, Av. Bandeirantes 3900, 14049-900 Ribeirão Preto, SP, Brazil.</nlm:affiliation></affiliation></author><author><name sortKey="Padovan Neto, Fernando E" sort="Padovan Neto, Fernando E" uniqKey="Padovan Neto F" first="Fernando E" last="Padovan-Neto">Fernando E. Padovan-Neto</name><affiliation><nlm:affiliation>USP, Center for Interdisciplinary Research on Applied Neurosciences (NAPNA), Brazil; USP, Department of Behavioral Neurosciences, Av. Bandeirantes 3900, 14049-900 Ribeirão Preto, SP, Brazil.</nlm:affiliation></affiliation></author><author><name sortKey="Da Silva, Celia Aparecida" sort="Da Silva, Celia Aparecida" uniqKey="Da Silva C" first="Célia Aparecida" last="Da-Silva">Célia Aparecida Da-Silva</name><affiliation><nlm:affiliation>University of São Paulo (USP), School of Odontology of Ribeirao Preto, Department of Morphology, Physiology and Basic Pathology, Av. Café S/N, 14040-904 Ribeirão Preto, SP, Brazil; USP, Center for Interdisciplinary Research on Applied Neurosciences (NAPNA), Brazil.</nlm:affiliation></affiliation></author><author><name sortKey="Mitkovski, Miso" sort="Mitkovski, Miso" uniqKey="Mitkovski M" first="Miso" last="Mitkovski">Miso Mitkovski</name><affiliation><nlm:affiliation>Light Microscopy Facility Max-Planck-Institute of Experimental Medicine, Hermann-Rein-Str. 3, 37075 Göttingen, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Raisman Vozari, Rita" sort="Raisman Vozari, Rita" uniqKey="Raisman Vozari R" first="Rita" last="Raisman-Vozari">Rita Raisman-Vozari</name><affiliation><nlm:affiliation>Sorbonne Université UPMC UM75 INSERM U1127, CNRS UMR 7225, Institut de Cerveau et de la Moelle Epinière, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Del Bel, Elaine" sort="Del Bel, Elaine" uniqKey="Del Bel E" first="Elaine" last="Del-Bel">Elaine Del-Bel</name><affiliation><nlm:affiliation>University of São Paulo (USP), School of Odontology of Ribeirao Preto, Department of Morphology, Physiology and Basic Pathology, Av. Café S/N, 14040-904 Ribeirão Preto, SP, Brazil; USP, Center for Interdisciplinary Research on Applied Neurosciences (NAPNA), Brazil; USP, Medical School, Department of Physiology, Av. Bandeirantes 3900, 14049-900 Ribeirão Preto, SP, Brazil; USP, Department of Behavioral Neurosciences, Av. Bandeirantes 3900, 14049-900 Ribeirão Preto, SP, Brazil. Electronic address: eadelbel@forp.usp.br.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Neurobiology of disease</title><idno type="eISSN">1095-953X</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antiparkinson Agents (adverse effects)</term><term>Disease Models, Animal</term><term>Dyskinesia, Drug-Induced (drug therapy)</term><term>Dyskinesia, Drug-Induced (metabolism)</term><term>Indazoles (pharmacology)</term><term>Inflammation (chemically induced)</term><term>Levodopa (administration & dosage)</term><term>Levodopa (adverse effects)</term><term>Male</term><term>Neuroglia (metabolism)</term><term>Neuroprotective Agents (pharmacology)</term><term>Nitric Oxide (metabolism)</term><term>Nitric Oxide Synthase (antagonists & inhibitors)</term><term>Parkinson Disease (drug therapy)</term><term>Rats</term><term>Rats, Wistar</term><term>Up-Regulation</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Nitric Oxide Synthase</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>Neuroglia</term><term>Nitric Oxide</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Indazoles</term><term>Neuroprotective Agents</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Male</term><term>Rats</term><term>Rats, Wistar</term><term>Up-Regulation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">l-3, 4-dihydroxyphenylalanine (L-DOPA) is the most effective treatment for Parkinson's disease but can induce debilitating abnormal involuntary movements (dyskinesia). Here we show that the development of L-DOPA-induced dyskinesia in the rat is accompanied by upregulation of an inflammatory cascade involving nitric oxide. Male Wistar rats sustained unilateral injections of 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle. After three weeks animals started to receive daily treatment with L-DOPA (30 mg/kg plus benserazide 7.5 mg/kg, for 21 days), combined with an inhibitor of neuronal NOS (7-nitroindazole, 7-NI, 30 mg/kg/day) or vehicle (saline-PEG 50%). All animals treated with L-DOPA and vehicle developed abnormal involuntary movements, and this effect was prevented by 7-NI. L-DOPA-treated dyskinetic animals exhibited an increased striatal and pallidal expression of glial fibrillary acidic protein (GFAP) in reactive astrocytes, an increased number of CD11b-positive microglial cells with activated morphology, and the rise of cells positive for inducible nitric oxide-synthase immunoreactivity (iNOS). All these indexes of glial activation were prevented by 7-NI co-administration. These findings provide evidence that the development of L-DOPA-induced dyskinesia in the rat is associated with activation of glial cells that promote inflammatory responses. The dramatic effect of 7-NI in preventing this glial response points to an involvement of nitric oxide. Moreover, the results suggest that the NOS inhibitor prevents dyskinesia at least in part via inhibition of glial cell activation and iNOS expression. Our observations indicate nitric oxide synthase inhibitors as a therapeutic strategy for preventing neuroinflammatory and glial components of dyskinesia pathogenesis in Parkinson's disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25447229</PMID><DateCreated><Year>2015</Year><Month>10</Month><Day>07</Day></DateCreated><DateCompleted><Year>2016</Year><Month>08</Month><Day>29</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1095-953X</ISSN><JournalIssue CitedMedium="Internet"><Volume>73</Volume><PubDate><Year>2015</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Neurobiology of disease</Title><ISOAbbreviation>Neurobiol. Dis.</ISOAbbreviation></Journal><ArticleTitle>Glial activation is associated with l-DOPA induced dyskinesia and blocked by a nitric oxide synthase inhibitor in a rat model of Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>377-87</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.nbd.2014.10.017</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0969-9961(14)00330-1</ELocationID><Abstract><AbstractText>l-3, 4-dihydroxyphenylalanine (L-DOPA) is the most effective treatment for Parkinson's disease but can induce debilitating abnormal involuntary movements (dyskinesia). Here we show that the development of L-DOPA-induced dyskinesia in the rat is accompanied by upregulation of an inflammatory cascade involving nitric oxide. Male Wistar rats sustained unilateral injections of 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle. After three weeks animals started to receive daily treatment with L-DOPA (30 mg/kg plus benserazide 7.5 mg/kg, for 21 days), combined with an inhibitor of neuronal NOS (7-nitroindazole, 7-NI, 30 mg/kg/day) or vehicle (saline-PEG 50%). All animals treated with L-DOPA and vehicle developed abnormal involuntary movements, and this effect was prevented by 7-NI. L-DOPA-treated dyskinetic animals exhibited an increased striatal and pallidal expression of glial fibrillary acidic protein (GFAP) in reactive astrocytes, an increased number of CD11b-positive microglial cells with activated morphology, and the rise of cells positive for inducible nitric oxide-synthase immunoreactivity (iNOS). All these indexes of glial activation were prevented by 7-NI co-administration. These findings provide evidence that the development of L-DOPA-induced dyskinesia in the rat is associated with activation of glial cells that promote inflammatory responses. The dramatic effect of 7-NI in preventing this glial response points to an involvement of nitric oxide. Moreover, the results suggest that the NOS inhibitor prevents dyskinesia at least in part via inhibition of glial cell activation and iNOS expression. Our observations indicate nitric oxide synthase inhibitors as a therapeutic strategy for preventing neuroinflammatory and glial components of dyskinesia pathogenesis in Parkinson's disease.</AbstractText><CopyrightInformation>Copyright © 2015 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bortolanza</LastName><ForeName>Mariza</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>University of São Paulo (USP), School of Odontology of Ribeirao Preto, Department of Morphology, Physiology and Basic Pathology, Av. Café S/N, 14040-904 Ribeirão Preto, SP, Brazil; USP, Center for Interdisciplinary Research on Applied Neurosciences (NAPNA), Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cavalcanti-Kiwiatkoski</LastName><ForeName>Roberta</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>USP, Center for Interdisciplinary Research on Applied Neurosciences (NAPNA), Brazil; USP, Medical School, Department of Physiology, Av. Bandeirantes 3900, 14049-900 Ribeirão Preto, SP, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Padovan-Neto</LastName><ForeName>Fernando E</ForeName><Initials>FE</Initials><AffiliationInfo><Affiliation>USP, Center for Interdisciplinary Research on Applied Neurosciences (NAPNA), Brazil; USP, Department of Behavioral Neurosciences, Av. Bandeirantes 3900, 14049-900 Ribeirão Preto, SP, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>da-Silva</LastName><ForeName>Célia Aparecida</ForeName><Initials>CA</Initials><AffiliationInfo><Affiliation>University of São Paulo (USP), School of Odontology of Ribeirao Preto, Department of Morphology, Physiology and Basic Pathology, Av. Café S/N, 14040-904 Ribeirão Preto, SP, Brazil; USP, Center for Interdisciplinary Research on Applied Neurosciences (NAPNA), Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mitkovski</LastName><ForeName>Miso</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Light Microscopy Facility Max-Planck-Institute of Experimental Medicine, Hermann-Rein-Str. 3, 37075 Göttingen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Raisman-Vozari</LastName><ForeName>Rita</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Sorbonne Université UPMC UM75 INSERM U1127, CNRS UMR 7225, Institut de Cerveau et de la Moelle Epinière, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Del-Bel</LastName><ForeName>Elaine</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>University of São Paulo (USP), School of Odontology of Ribeirao Preto, Department of Morphology, Physiology and Basic Pathology, Av. Café S/N, 14040-904 Ribeirão Preto, SP, Brazil; USP, Center for Interdisciplinary Research on Applied Neurosciences (NAPNA), Brazil; USP, Medical School, Department of Physiology, Av. Bandeirantes 3900, 14049-900 Ribeirão Preto, SP, Brazil; USP, Department of Behavioral Neurosciences, Av. Bandeirantes 3900, 14049-900 Ribeirão Preto, SP, Brazil. Electronic address: eadelbel@forp.usp.br.</Affiliation></AffiliationInfo></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>2014</Year><Month>10</Month><Day>30</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="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007191">Indazoles</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018696">Neuroprotective 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Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004409" MajorTopicYN="N">Dyskinesia, Drug-Induced</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007191" MajorTopicYN="N">Indazoles</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007980" MajorTopicYN="N">Levodopa</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009457" MajorTopicYN="N">Neuroglia</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018696" MajorTopicYN="N">Neuroprotective Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009569" MajorTopicYN="N">Nitric Oxide</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019001" MajorTopicYN="N">Nitric Oxide Synthase</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017208" MajorTopicYN="N">Rats, Wistar</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015854" MajorTopicYN="N">Up-Regulation</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">6-OHDA lesion</Keyword><Keyword MajorTopicYN="N">GFAP</Keyword><Keyword MajorTopicYN="N">Glial cells</Keyword><Keyword MajorTopicYN="N">Neuroinflammation</Keyword><Keyword MajorTopicYN="N">OX-42</Keyword><Keyword MajorTopicYN="N">iNOS</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>09</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>10</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>12</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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