mGlu5 receptor antagonist blocks bromocriptine-induced conditioned place preference in bilateral mesolimbic-lesioned rat.
Identifieur interne : 000021 ( PubMed/Curation ); précédent : 000020; suivant : 000022mGlu5 receptor antagonist blocks bromocriptine-induced conditioned place preference in bilateral mesolimbic-lesioned rat.
Auteurs : Omar Ouachikh [France] ; Carine Chassain [France] ; Guilhem Pagès [France] ; Franck Durif [France] ; Aziz Hafidi [France]Source :
- Behavioural brain research [ 1872-7549 ] ; 2017.
Abstract
Dopamine dysregulation syndrome (DDS) has been attributed to both dopamine replacement therapies (DRT) and the mesencephalic dopaminergic lesion. The DRT reinforcement effect is due to its action on the reward system, particularly on the nucleus accumbens (NAc). This nucleus receives two major projections, a glutamatergic from the prefrontal cortex and a dopaminergic from the posterior ventral tegmental area (pVTA). The latter modulate the former within the NAc. pVTA has been demonstrated to be implicated in the motivational effect of bromocriptine (dopamine 2 receptor (D2R) agonist) in bilateral pVTA-lesioned animals. Therefore the potential implication of the metabotropic glutamate receptor 5 (mGluR5) antagonist (MTEP: 3-((2-Methyl-1,3-thiazol-4-yl)ethynyl)pyridine) on bromocriptine-induced conditioned place preference (CPP) was explored. Results showed that the administration of the MTEP blocked completely the bromocriptine-induced CPP in bilateral pVTA-lesioned rats. Both the CPP acquisition and expression were abolished. These effects are due, at least to an increase of the glutamate concentration and that of mGlu5 receptor expression in the NAc shell of the pVTA-lesioned animals. Altogether these data demonstrated the importance of the mGlu5 receptor in the bromocriptine induced-reinforcement and that DDS is probably due to DRT effect on this glutamate receptor.
DOI: 10.1016/j.bbr.2016.09.030
PubMed: 27638036
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Electronic address: azhafidi@univ-bpclermont.fr.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Clermont Université, Université d'Auvergne, EA7280, Laboratoire de Neuropsychopharmacologie des systèmes dopaminergiques sous corticaux, Clermont-Ferrand</wicri:regionArea></affiliation></author></analytic><series><title level="j">Behavioural brain research</title><idno type="eISSN">1872-7549</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Dopamine dysregulation syndrome (DDS) has been attributed to both dopamine replacement therapies (DRT) and the mesencephalic dopaminergic lesion. The DRT reinforcement effect is due to its action on the reward system, particularly on the nucleus accumbens (NAc). This nucleus receives two major projections, a glutamatergic from the prefrontal cortex and a dopaminergic from the posterior ventral tegmental area (pVTA). The latter modulate the former within the NAc. pVTA has been demonstrated to be implicated in the motivational effect of bromocriptine (dopamine 2 receptor (D2R) agonist) in bilateral pVTA-lesioned animals. Therefore the potential implication of the metabotropic glutamate receptor 5 (mGluR5) antagonist (MTEP: 3-((2-Methyl-1,3-thiazol-4-yl)ethynyl)pyridine) on bromocriptine-induced conditioned place preference (CPP) was explored. Results showed that the administration of the MTEP blocked completely the bromocriptine-induced CPP in bilateral pVTA-lesioned rats. Both the CPP acquisition and expression were abolished. These effects are due, at least to an increase of the glutamate concentration and that of mGlu5 receptor expression in the NAc shell of the pVTA-lesioned animals. Altogether these data demonstrated the importance of the mGlu5 receptor in the bromocriptine induced-reinforcement and that DDS is probably due to DRT effect on this glutamate receptor.</div></front></TEI><pubmed><MedlineCitation Status="In-Data-Review" Owner="NLM"><PMID Version="1">27638036</PMID><DateCreated><Year>2016</Year><Month>09</Month><Day>17</Day></DateCreated><DateRevised><Year>2016</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-7549</ISSN><JournalIssue CitedMedium="Internet"><Volume>317</Volume><PubDate><Year>2017</Year><Month>Jan</Month><Day>15</Day></PubDate></JournalIssue><Title>Behavioural brain research</Title><ISOAbbreviation>Behav. Brain Res.</ISOAbbreviation></Journal><ArticleTitle>mGlu5 receptor antagonist blocks bromocriptine-induced conditioned place preference in bilateral mesolimbic-lesioned rat.</ArticleTitle><Pagination><MedlinePgn>301-310</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0166-4328(16)30613-1</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bbr.2016.09.030</ELocationID><Abstract><AbstractText NlmCategory="UNASSIGNED">Dopamine dysregulation syndrome (DDS) has been attributed to both dopamine replacement therapies (DRT) and the mesencephalic dopaminergic lesion. The DRT reinforcement effect is due to its action on the reward system, particularly on the nucleus accumbens (NAc). This nucleus receives two major projections, a glutamatergic from the prefrontal cortex and a dopaminergic from the posterior ventral tegmental area (pVTA). The latter modulate the former within the NAc. pVTA has been demonstrated to be implicated in the motivational effect of bromocriptine (dopamine 2 receptor (D2R) agonist) in bilateral pVTA-lesioned animals. Therefore the potential implication of the metabotropic glutamate receptor 5 (mGluR5) antagonist (MTEP: 3-((2-Methyl-1,3-thiazol-4-yl)ethynyl)pyridine) on bromocriptine-induced conditioned place preference (CPP) was explored. Results showed that the administration of the MTEP blocked completely the bromocriptine-induced CPP in bilateral pVTA-lesioned rats. Both the CPP acquisition and expression were abolished. These effects are due, at least to an increase of the glutamate concentration and that of mGlu5 receptor expression in the NAc shell of the pVTA-lesioned animals. Altogether these data demonstrated the importance of the mGlu5 receptor in the bromocriptine induced-reinforcement and that DDS is probably due to DRT effect on this glutamate receptor.</AbstractText><CopyrightInformation>Copyright © 2016. Published by Elsevier B.V.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ouachikh</LastName><ForeName>Omar</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Clermont Université, Université d'Auvergne, EA7280, Laboratoire de Neuropsychopharmacologie des systèmes dopaminergiques sous corticaux, Clermont-Ferrand, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chassain</LastName><ForeName>Carine</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Clermont Université, Université d'Auvergne, EA7280, Laboratoire de Neuropsychopharmacologie des systèmes dopaminergiques sous corticaux, Clermont-Ferrand, France; CHU Clermont-Ferrand, Service de Neurologie, 63000 Clermont-Ferrand, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pagès</LastName><ForeName>Guilhem</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>2NMR platform "AgroResonance", UR370 Qualité des produits animaux (QuaPA), INRA-Centre, Auvergne-Rhône-Alpes, 63122 Saint-Genès Champanelle, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Durif</LastName><ForeName>Franck</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Clermont Université, Université d'Auvergne, EA7280, Laboratoire de Neuropsychopharmacologie des systèmes dopaminergiques sous corticaux, Clermont-Ferrand, France; CHU Clermont-Ferrand, Service de Neurologie, 63000 Clermont-Ferrand, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hafidi</LastName><ForeName>Aziz</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Clermont Université, Université d'Auvergne, EA7280, Laboratoire de Neuropsychopharmacologie des systèmes dopaminergiques sous corticaux, Clermont-Ferrand, France. Electronic address: azhafidi@univ-bpclermont.fr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>09</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Behav Brain Res</MedlineTA><NlmUniqueID>8004872</NlmUniqueID><ISSNLinking>0166-4328</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">6-OHDA</Keyword><Keyword MajorTopicYN="N">Conditioned place preference</Keyword><Keyword MajorTopicYN="N">Parkinson</Keyword><Keyword MajorTopicYN="N">Reward</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>05</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>09</Month><Day>06</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>09</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>10</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>10</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>9</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27638036</ArticleId><ArticleId IdType="pii">S0166-4328(16)30613-1</ArticleId><ArticleId IdType="doi">10.1016/j.bbr.2016.09.030</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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