Increasing levels of the endocannabinoid 2-AG is neuroprotective in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease.
Identifieur interne : 000489 ( PubMed/Checkpoint ); précédent : 000488; suivant : 000490Increasing levels of the endocannabinoid 2-AG is neuroprotective in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease.
Auteurs : Ross B. Mounsey [Royaume-Uni] ; Sarah Mustafa [Royaume-Uni] ; Lianne Robinson [Royaume-Uni] ; Ruth A. Ross [Canada] ; Gernot Riedel [Royaume-Uni] ; Roger G. Pertwee [Royaume-Uni] ; Peter Teismann [Royaume-Uni]Source :
- Experimental neurology [ 1090-2430 ] ; 2015.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (pharmacology), Animals, Arachidonic Acids (therapeutic use), Benzodioxoles (therapeutic use), Brain (drug effects), Brain (metabolism), Brain (pathology), Cell Death (drug effects), Cyclooxygenase 2 (metabolism), Disease Models, Animal, Dose-Response Relationship, Drug, Endocannabinoids (therapeutic use), Enzyme Inhibitors (pharmacology), Furans (therapeutic use), Gait Disorders, Neurologic (drug therapy), Gait Disorders, Neurologic (etiology), Glycerides (therapeutic use), Male, Mice, Mice, Inbred C57BL, Motor Activity (drug effects), Neuroprotective Agents (therapeutic use), Neurotoxins (toxicity), Parkinson Disease (complications), Parkinson Disease (diet therapy), Parkinson Disease (etiology), Parkinson Disease (pathology), Piperidines (therapeutic use), Time Factors, Tyrosine 3-Monooxygenase (metabolism).
- MESH :
- chemical , metabolism : Cyclooxygenase 2, Tyrosine 3-Monooxygenase.
- chemical , pharmacology : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Enzyme Inhibitors.
- chemical , therapeutic use : Arachidonic Acids, Benzodioxoles, Endocannabinoids, Furans, Glycerides, Neuroprotective Agents, Piperidines.
- complications : Parkinson Disease.
- diet therapy : Parkinson Disease.
- drug effects : Brain, Cell Death, Motor Activity.
- drug therapy : Gait Disorders, Neurologic.
- etiology : Gait Disorders, Neurologic, Parkinson Disease.
- metabolism : Brain.
- pathology : Brain, Parkinson Disease.
- chemical , toxicity : Neurotoxins.
- Animals, Disease Models, Animal, Dose-Response Relationship, Drug, Male, Mice, Mice, Inbred C57BL, Time Factors.
Abstract
Parkinson's disease (PD) is a common chronic neurodegenerative disorder, usually of idiopathic origin. Symptoms including tremor, bradykinesia, rigidity and postural instability are caused by the progressive loss of dopaminergic neurons in the nigrostriatal region of the brain. Symptomatic therapies are available but no treatment slows or prevents the loss of neurons. Neuroinflammation has been implicated in its pathogenesis. To this end, the present study utilises the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxin to reproduce the pattern of cell death evident in PD patients. Herein, the role of a potential regulator of an immune response, the endocannabinoid system (ECS), is investigated. The most prevalent endocannabinoid, 2-arachidonoylglycerol (2-AG) (3 and 5mg/kg), was added exogenously and its enzymatic degradation inhibited to provide protection against MPTP-induced cell death. Furthermore, the addition of DFU (25mg/kg), a selective inhibitor of inflammatory mediator cyclooxygenase-2 (COX-2), potentiated these effects. Levels of 2-AG were shown to be upregulated in a time- and region-specific manner following MPTP administration, indicating that the ECS represents a natural defence mechanism against inflammation, potentiation of which could provide therapeutic benefits. The results expand the current understanding of the role that this signalling system has and its potential influence in PD.
DOI: 10.1016/j.expneurol.2015.07.024
PubMed: 26244281
Affiliations:
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Ross</name><affiliation wicri:level="4"><nlm:affiliation>Department of Pharmacology and Toxicology, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario M5S 1A, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Pharmacology and Toxicology, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario M5S 1A</wicri:regionArea><orgName type="university">Université de Toronto</orgName><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName></affiliation></author><author><name sortKey="Riedel, Gernot" sort="Riedel, Gernot" uniqKey="Riedel G" first="Gernot" last="Riedel">Gernot Riedel</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD Scotland, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD Scotland</wicri:regionArea><wicri:noRegion>AB25 2ZD Scotland</wicri:noRegion></affiliation></author><author><name sortKey="Pertwee, Roger G" sort="Pertwee, Roger G" uniqKey="Pertwee R" first="Roger G" last="Pertwee">Roger G. 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Electronic address: p.teismann@abdn.ac.uk.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD Scotland</wicri:regionArea><wicri:noRegion>AB25 2ZD Scotland</wicri:noRegion></affiliation></author></analytic><series><title level="j">Experimental neurology</title><idno type="eISSN">1090-2430</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (pharmacology)</term><term>Animals</term><term>Arachidonic Acids (therapeutic use)</term><term>Benzodioxoles (therapeutic use)</term><term>Brain (drug effects)</term><term>Brain (metabolism)</term><term>Brain (pathology)</term><term>Cell Death (drug effects)</term><term>Cyclooxygenase 2 (metabolism)</term><term>Disease Models, Animal</term><term>Dose-Response Relationship, Drug</term><term>Endocannabinoids (therapeutic use)</term><term>Enzyme Inhibitors (pharmacology)</term><term>Furans (therapeutic use)</term><term>Gait Disorders, Neurologic (drug therapy)</term><term>Gait Disorders, Neurologic (etiology)</term><term>Glycerides (therapeutic use)</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Motor Activity (drug effects)</term><term>Neuroprotective Agents (therapeutic use)</term><term>Neurotoxins (toxicity)</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (diet therapy)</term><term>Parkinson Disease (etiology)</term><term>Parkinson Disease (pathology)</term><term>Piperidines (therapeutic use)</term><term>Time Factors</term><term>Tyrosine 3-Monooxygenase (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cyclooxygenase 2</term><term>Tyrosine 3-Monooxygenase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Enzyme Inhibitors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Arachidonic Acids</term><term>Benzodioxoles</term><term>Endocannabinoids</term><term>Furans</term><term>Glycerides</term><term>Neuroprotective Agents</term><term>Piperidines</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="diet therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Brain</term><term>Cell Death</term><term>Motor Activity</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Gait Disorders, Neurologic</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Gait Disorders, Neurologic</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Neurotoxins</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Dose-Response Relationship, Drug</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Time Factors</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a common chronic neurodegenerative disorder, usually of idiopathic origin. Symptoms including tremor, bradykinesia, rigidity and postural instability are caused by the progressive loss of dopaminergic neurons in the nigrostriatal region of the brain. Symptomatic therapies are available but no treatment slows or prevents the loss of neurons. Neuroinflammation has been implicated in its pathogenesis. To this end, the present study utilises the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxin to reproduce the pattern of cell death evident in PD patients. Herein, the role of a potential regulator of an immune response, the endocannabinoid system (ECS), is investigated. The most prevalent endocannabinoid, 2-arachidonoylglycerol (2-AG) (3 and 5mg/kg), was added exogenously and its enzymatic degradation inhibited to provide protection against MPTP-induced cell death. Furthermore, the addition of DFU (25mg/kg), a selective inhibitor of inflammatory mediator cyclooxygenase-2 (COX-2), potentiated these effects. Levels of 2-AG were shown to be upregulated in a time- and region-specific manner following MPTP administration, indicating that the ECS represents a natural defence mechanism against inflammation, potentiation of which could provide therapeutic benefits. The results expand the current understanding of the role that this signalling system has and its potential influence in PD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26244281</PMID><DateCreated><Year>2015</Year><Month>11</Month><Day>13</Day></DateCreated><DateCompleted><Year>2016</Year><Month>02</Month><Day>18</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1090-2430</ISSN><JournalIssue CitedMedium="Internet"><Volume>273</Volume><PubDate><Year>2015</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Experimental neurology</Title><ISOAbbreviation>Exp. Neurol.</ISOAbbreviation></Journal><ArticleTitle>Increasing levels of the endocannabinoid 2-AG is neuroprotective in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>36-44</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.expneurol.2015.07.024</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0014-4886(15)30058-3</ELocationID><Abstract><AbstractText>Parkinson's disease (PD) is a common chronic neurodegenerative disorder, usually of idiopathic origin. Symptoms including tremor, bradykinesia, rigidity and postural instability are caused by the progressive loss of dopaminergic neurons in the nigrostriatal region of the brain. Symptomatic therapies are available but no treatment slows or prevents the loss of neurons. Neuroinflammation has been implicated in its pathogenesis. To this end, the present study utilises the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxin to reproduce the pattern of cell death evident in PD patients. Herein, the role of a potential regulator of an immune response, the endocannabinoid system (ECS), is investigated. The most prevalent endocannabinoid, 2-arachidonoylglycerol (2-AG) (3 and 5mg/kg), was added exogenously and its enzymatic degradation inhibited to provide protection against MPTP-induced cell death. Furthermore, the addition of DFU (25mg/kg), a selective inhibitor of inflammatory mediator cyclooxygenase-2 (COX-2), potentiated these effects. Levels of 2-AG were shown to be upregulated in a time- and region-specific manner following MPTP administration, indicating that the ECS represents a natural defence mechanism against inflammation, potentiation of which could provide therapeutic benefits. The results expand the current understanding of the role that this signalling system has and its potential influence in PD.</AbstractText><CopyrightInformation>Copyright © 2015. Published by Elsevier Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mounsey</LastName><ForeName>Ross B</ForeName><Initials>RB</Initials><AffiliationInfo><Affiliation>Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD Scotland, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mustafa</LastName><ForeName>Sarah</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD Scotland, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Robinson</LastName><ForeName>Lianne</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD Scotland, UK; Ninewells Hospital and Medical School, University of Dundee, Dundee, DD1 9SY Scotland, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ross</LastName><ForeName>Ruth A</ForeName><Initials>RA</Initials><AffiliationInfo><Affiliation>Department of Pharmacology and Toxicology, University of Toronto, Medical Sciences Building, 1 King's College Circle, Toronto, Ontario M5S 1A, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Riedel</LastName><ForeName>Gernot</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD Scotland, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pertwee</LastName><ForeName>Roger G</ForeName><Initials>RG</Initials><AffiliationInfo><Affiliation>Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD Scotland, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Teismann</LastName><ForeName>Peter</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD Scotland, UK. Electronic address: p.teismann@abdn.ac.uk.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>WT080782MF</GrantID><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>08</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Exp Neurol</MedlineTA><NlmUniqueID>0370712</NlmUniqueID><ISSNLinking>0014-4886</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C106876">5,5-dimethyl-3-(3-fluorophenyl)-4-(4-methylsulfonyl)phenyl-2(5H)-furanone</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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UI="D009498">Neurotoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010880">Piperidines</NameOfSubstance></Chemical><Chemical><RegistryNumber>8D239QDW64</RegistryNumber><NameOfSubstance UI="C094503">glyceryl 2-arachidonate</NameOfSubstance></Chemical><Chemical><RegistryNumber>9P21XSP91P</RegistryNumber><NameOfSubstance UI="D015632">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.16.2</RegistryNumber><NameOfSubstance UI="D014446">Tyrosine 3-Monooxygenase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.99.1</RegistryNumber><NameOfSubstance UI="D051546">Cyclooxygenase 2</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Neurosci Lett. 1995 Dec 29;202(1-2):17-20</RefSource><PMID Version="1">8787820</PMID></CommentsCorrections><CommentsCorrections 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PubStatus="revised"><Year>2015</Year><Month>06</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>07</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>8</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>8</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>2</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26244281</ArticleId><ArticleId IdType="pii">S0014-4886(15)30058-3</ArticleId><ArticleId IdType="doi">10.1016/j.expneurol.2015.07.024</ArticleId><ArticleId IdType="pmc">PMC4654430</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li><li>Royaume-Uni</li></country><region><li>Ontario</li></region><settlement><li>Toronto</li></settlement><orgName><li>Université de Toronto</li></orgName></list><tree><country name="Royaume-Uni"><noRegion><name sortKey="Mounsey, Ross B" sort="Mounsey, Ross B" uniqKey="Mounsey R" first="Ross B" last="Mounsey">Ross B. Mounsey</name></noRegion><name sortKey="Mustafa, Sarah" sort="Mustafa, Sarah" uniqKey="Mustafa S" first="Sarah" last="Mustafa">Sarah Mustafa</name><name sortKey="Pertwee, Roger G" sort="Pertwee, Roger G" uniqKey="Pertwee R" first="Roger G" last="Pertwee">Roger G. Pertwee</name><name sortKey="Riedel, Gernot" sort="Riedel, Gernot" uniqKey="Riedel G" first="Gernot" last="Riedel">Gernot Riedel</name><name sortKey="Robinson, Lianne" sort="Robinson, Lianne" uniqKey="Robinson L" first="Lianne" last="Robinson">Lianne Robinson</name><name sortKey="Teismann, Peter" sort="Teismann, Peter" uniqKey="Teismann P" first="Peter" last="Teismann">Peter Teismann</name></country><country name="Canada"><region name="Ontario"><name sortKey="Ross, Ruth A" sort="Ross, Ruth A" uniqKey="Ross R" first="Ruth A" last="Ross">Ruth A. Ross</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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