The role of parkinson's disease-associated receptor GPR37 in the hippocampus: functional interplay with the adenosinergic system.
Identifieur interne : 000473 ( PubMed/Curation ); précédent : 000472; suivant : 000474The role of parkinson's disease-associated receptor GPR37 in the hippocampus: functional interplay with the adenosinergic system.
Auteurs : João P. Lopes [Portugal] ; Xavier Morat [Espagne] ; Carolina Souza [Portugal] ; Cindy Pinhal [Portugal] ; Nuno J. Machado [Portugal] ; Paula M. Canas [Portugal] ; Henrique B. Silva [Portugal] ; Igor Stagljar [Canada] ; Jorge Gandía [Espagne] ; Víctor Fernández-Due As [Espagne] ; Rafael Luján [Espagne] ; Rodrigo A. Cunha [Portugal] ; Francisco Ciruela [Espagne]Source :
- Journal of neurochemistry [ 1471-4159 ] ; 2015.
English descriptors
- KwdEn :
- Animals, Anxiety (metabolism), Cells, Cultured, HEK293 Cells, Hippocampus (chemistry), Hippocampus (metabolism), Humans, Long-Term Potentiation (physiology), Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Parkinson Disease (metabolism), Receptor, Adenosine A2A (analysis), Receptor, Adenosine A2A (metabolism), Receptors, G-Protein-Coupled (analysis), Receptors, G-Protein-Coupled (physiology).
- MESH :
- chemical , analysis : Receptor, Adenosine A2A, Receptors, G-Protein-Coupled.
- chemistry : Hippocampus.
- metabolism : Anxiety, Hippocampus, Parkinson Disease, Receptor, Adenosine A2A.
- physiology : Long-Term Potentiation, Receptors, G-Protein-Coupled.
- Animals, Cells, Cultured, HEK293 Cells, Humans, Male, Mice, Mice, Inbred C57BL, Mice, Knockout.
Abstract
GPR37 is an orphan G protein-coupled receptor mostly enriched in brain areas such as the cerebellum, striatum, and hippocampus. Identified as a substrate of parkin, GPR37 has been suggested to play a role in Parkinson's disease. Distributed throughout the brain, the function of GPR37, however, remains unknown. We now provide the first mapping of GPR37 within the hippocampus, where GPR37 is widely expressed and localized at the level of the extrasynaptic plasma membrane of dendritic spines, dendritic shafts, and axon terminals. GPR37 per se does not appear to play a role in learning and memory, since knocking out GPR37 (GPR37-KO) did not alter the performance in different hippocampal-related memory tasks. This is in agreement with slice electrophysiology experiments showing no differences both in short-term plasticity paired-pulse facilitation and long-term potentiation between WT and GPR37-KO mice. However, we report a potential functional interaction between GPR37 and adenosine A2A receptors (A2 A R) in the hippocampus, with A2 A R modulating the GPR37-associated phenotype. Thus, the absence of GPR37 appeared to sensitize mice to hippocampal A2 A R-mediated signaling, as observed by the effect of the A2 A R antagonist SCH58261 increasing synaptic depotentiation, reducing novel object recognition memory and reverting the anxiolytic effect of GPR37 deletion. Collectively, these findings afford insight into the localization and role of the orphan GPR37 within the hippocampus with potential involvement in A2 A R function (i.e., A2 A R sensitization). GPR37 is an orphan G protein-coupled receptor widely expressed in the hippocampus and localized at the level of the extrasynaptic plasma membrane of dendritic spines, dendritic shafts and axon terminals. This orphan receptor per se does not appear to directly control the learning and memory processes; however knocking-out GPR37 triggers anxiolytic-like effects and sensitizes mice to hippocampal A2A R-mediated signalling.
DOI: 10.1111/jnc.13109
PubMed: 25824528
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<term>Cells, Cultured</term>
<term>HEK293 Cells</term>
<term>Hippocampus (chemistry)</term>
<term>Hippocampus (metabolism)</term>
<term>Humans</term>
<term>Long-Term Potentiation (physiology)</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Parkinson Disease (metabolism)</term>
<term>Receptor, Adenosine A2A (analysis)</term>
<term>Receptor, Adenosine A2A (metabolism)</term>
<term>Receptors, G-Protein-Coupled (analysis)</term>
<term>Receptors, G-Protein-Coupled (physiology)</term>
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<term>Hippocampus</term>
<term>Parkinson Disease</term>
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<front><div type="abstract" xml:lang="en">GPR37 is an orphan G protein-coupled receptor mostly enriched in brain areas such as the cerebellum, striatum, and hippocampus. Identified as a substrate of parkin, GPR37 has been suggested to play a role in Parkinson's disease. Distributed throughout the brain, the function of GPR37, however, remains unknown. We now provide the first mapping of GPR37 within the hippocampus, where GPR37 is widely expressed and localized at the level of the extrasynaptic plasma membrane of dendritic spines, dendritic shafts, and axon terminals. GPR37 per se does not appear to play a role in learning and memory, since knocking out GPR37 (GPR37-KO) did not alter the performance in different hippocampal-related memory tasks. This is in agreement with slice electrophysiology experiments showing no differences both in short-term plasticity paired-pulse facilitation and long-term potentiation between WT and GPR37-KO mice. However, we report a potential functional interaction between GPR37 and adenosine A2A receptors (A2 A R) in the hippocampus, with A2 A R modulating the GPR37-associated phenotype. Thus, the absence of GPR37 appeared to sensitize mice to hippocampal A2 A R-mediated signaling, as observed by the effect of the A2 A R antagonist SCH58261 increasing synaptic depotentiation, reducing novel object recognition memory and reverting the anxiolytic effect of GPR37 deletion. Collectively, these findings afford insight into the localization and role of the orphan GPR37 within the hippocampus with potential involvement in A2 A R function (i.e., A2 A R sensitization). GPR37 is an orphan G protein-coupled receptor widely expressed in the hippocampus and localized at the level of the extrasynaptic plasma membrane of dendritic spines, dendritic shafts and axon terminals. This orphan receptor per se does not appear to directly control the learning and memory processes; however knocking-out GPR37 triggers anxiolytic-like effects and sensitizes mice to hippocampal A2A R-mediated signalling.</div>
</front>
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<ELocationID EIdType="doi" ValidYN="Y">10.1111/jnc.13109</ELocationID>
<Abstract><AbstractText>GPR37 is an orphan G protein-coupled receptor mostly enriched in brain areas such as the cerebellum, striatum, and hippocampus. Identified as a substrate of parkin, GPR37 has been suggested to play a role in Parkinson's disease. Distributed throughout the brain, the function of GPR37, however, remains unknown. We now provide the first mapping of GPR37 within the hippocampus, where GPR37 is widely expressed and localized at the level of the extrasynaptic plasma membrane of dendritic spines, dendritic shafts, and axon terminals. GPR37 per se does not appear to play a role in learning and memory, since knocking out GPR37 (GPR37-KO) did not alter the performance in different hippocampal-related memory tasks. This is in agreement with slice electrophysiology experiments showing no differences both in short-term plasticity paired-pulse facilitation and long-term potentiation between WT and GPR37-KO mice. However, we report a potential functional interaction between GPR37 and adenosine A2A receptors (A2 A R) in the hippocampus, with A2 A R modulating the GPR37-associated phenotype. Thus, the absence of GPR37 appeared to sensitize mice to hippocampal A2 A R-mediated signaling, as observed by the effect of the A2 A R antagonist SCH58261 increasing synaptic depotentiation, reducing novel object recognition memory and reverting the anxiolytic effect of GPR37 deletion. Collectively, these findings afford insight into the localization and role of the orphan GPR37 within the hippocampus with potential involvement in A2 A R function (i.e., A2 A R sensitization). GPR37 is an orphan G protein-coupled receptor widely expressed in the hippocampus and localized at the level of the extrasynaptic plasma membrane of dendritic spines, dendritic shafts and axon terminals. This orphan receptor per se does not appear to directly control the learning and memory processes; however knocking-out GPR37 triggers anxiolytic-like effects and sensitizes mice to hippocampal A2A R-mediated signalling.</AbstractText>
<CopyrightInformation>© 2015 International Society for Neurochemistry.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lopes</LastName>
<ForeName>João P</ForeName>
<Initials>JP</Initials>
<AffiliationInfo><Affiliation>CNC-Center for Neurosciences and Cell Biology and Faculty of Medicine, University of Coimbra, Coimbra, Portugal.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Morató</LastName>
<ForeName>Xavier</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Unitat de Farmacologia, Departament Patologia i Terapèutica Experimental, Facultat de Medicina, IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Spain.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Souza</LastName>
<ForeName>Carolina</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>CNC-Center for Neurosciences and Cell Biology and Faculty of Medicine, University of Coimbra, Coimbra, Portugal.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Pinhal</LastName>
<ForeName>Cindy</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>CNC-Center for Neurosciences and Cell Biology and Faculty of Medicine, University of Coimbra, Coimbra, Portugal.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Machado</LastName>
<ForeName>Nuno J</ForeName>
<Initials>NJ</Initials>
<AffiliationInfo><Affiliation>CNC-Center for Neurosciences and Cell Biology and Faculty of Medicine, University of Coimbra, Coimbra, Portugal.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Canas</LastName>
<ForeName>Paula M</ForeName>
<Initials>PM</Initials>
<AffiliationInfo><Affiliation>CNC-Center for Neurosciences and Cell Biology and Faculty of Medicine, University of Coimbra, Coimbra, Portugal.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Silva</LastName>
<ForeName>Henrique B</ForeName>
<Initials>HB</Initials>
<AffiliationInfo><Affiliation>CNC-Center for Neurosciences and Cell Biology and Faculty of Medicine, University of Coimbra, Coimbra, Portugal.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Stagljar</LastName>
<ForeName>Igor</ForeName>
<Initials>I</Initials>
<AffiliationInfo><Affiliation>Department of Biochemistry and Department of Molecular Genetics, Donnelly Centre, University of Toronto, Toronto, Ontario, Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gandía</LastName>
<ForeName>Jorge</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Unitat de Farmacologia, Departament Patologia i Terapèutica Experimental, Facultat de Medicina, IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Spain.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Fernández-Dueñas</LastName>
<ForeName>Víctor</ForeName>
<Initials>V</Initials>
<AffiliationInfo><Affiliation>Unitat de Farmacologia, Departament Patologia i Terapèutica Experimental, Facultat de Medicina, IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Spain.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Luján</LastName>
<ForeName>Rafael</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Departamento de Ciencias Médicas, Instituto de Investigación en Discapacidades Neurológicas (IDINE), Facultad de Medicina, Universidad Castilla-La Mancha, Albacete, Spain.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Cunha</LastName>
<ForeName>Rodrigo A</ForeName>
<Initials>RA</Initials>
<AffiliationInfo><Affiliation>CNC-Center for Neurosciences and Cell Biology and Faculty of Medicine, University of Coimbra, Coimbra, Portugal.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Faculty of Medicine, University of Coimbra, Coimbra, Portugal.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ciruela</LastName>
<ForeName>Francisco</ForeName>
<Initials>F</Initials>
<AffiliationInfo><Affiliation>Unitat de Farmacologia, Departament Patologia i Terapèutica Experimental, Facultat de Medicina, IDIBELL, Universitat de Barcelona, L'Hospitalet de Llobregat, Spain.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Physiology, Faculty of Sciences, University of Ghent, Gent, Belgium.</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>2015</Year>
<Month>04</Month>
<Day>21</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>J Neurochem</MedlineTA>
<NlmUniqueID>2985190R</NlmUniqueID>
<ISSNLinking>0022-3042</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C509804">Gpr37 protein, mouse</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D043705">Receptor, Adenosine A2A</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D043562">Receptors, G-Protein-Coupled</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001007" MajorTopicYN="N">Anxiety</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D057809" MajorTopicYN="N">HEK293 Cells</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006624" MajorTopicYN="N">Hippocampus</DescriptorName>
<QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017774" MajorTopicYN="N">Long-Term Potentiation</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D043705" MajorTopicYN="N">Receptor, Adenosine A2A</DescriptorName>
<QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D043562" MajorTopicYN="N">Receptors, G-Protein-Coupled</DescriptorName>
<QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">GPR37</Keyword>
<Keyword MajorTopicYN="N">adenosine A2A receptor</Keyword>
<Keyword MajorTopicYN="N">hippocampus</Keyword>
<Keyword MajorTopicYN="N">synaptic plasticity</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year>
<Month>11</Month>
<Day>01</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2015</Year>
<Month>02</Month>
<Day>19</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2015</Year>
<Month>03</Month>
<Day>18</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2015</Year>
<Month>4</Month>
<Day>1</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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<PubMedPubDate PubStatus="pubmed"><Year>2015</Year>
<Month>4</Month>
<Day>1</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2015</Year>
<Month>9</Month>
<Day>10</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">25824528</ArticleId>
<ArticleId IdType="doi">10.1111/jnc.13109</ArticleId>
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