Increased amygdalar metabotropic glutamate receptor 7 mRNA in a genetic mouse model of impaired fear extinction

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dc.contributor.authorO’Connor, Richard M.en
dc.contributor.authorMcCafferty, Cian P.en
dc.contributor.authorBravo, Javier A.en
dc.contributor.authorSingewald, Nicolasen
dc.contributor.authorHolmes, Andrewen
dc.contributor.authorCryan, John F.en
dc.contributor.funderScience Foundation Irelanden
dc.contributor.funderHealth Research Boarden
dc.contributor.funderIrish Research Council for Science, Engineering and Technologyen
dc.contributor.funderNational Institute on Alcohol Abuse and Alcoholismen
dc.contributor.funderAustrian Science Funden
dc.date.accessioned2024-05-20T15:14:36Z
dc.date.available2024-05-20T15:14:36Z
dc.date.issued2018-09-13en
dc.description.abstractRationale: Post-traumatic stress disorder (PTSD) is a devastating anxiety-related disorder which develops subsequent to a severe psychologically traumatic event. Only ~ 9% of people who experience such a trauma develop PTSD. It is clear that a number of factors, including genetics, influence whether an individual will develop PTSD subsequent to a trauma. The 129S1/SvImJ (S1) inbred mouse strain displays poor fear extinction and may be useful to model this specific aspect of PTSD. The metabotropic glutamate receptor 7 (mGlu7 receptor) has previously been shown to be involved in cognitive processes and anxiety-like behaviour placing it in a key position to regulate fear extinction processes. We sought to compare mGlu7 receptor mRNA levels in the S1 strain with those in the robustly extinguishing C57BL/6J (B6) inbred strain using in situ hybridisation (ISH) in three brain regions associated with fear extinction: the amygdala, hippocampus and prefrontal cortex (PFC). Results: Compared to the B6 strain, S1 mice had increased mGlu7 receptor mRNA levels in the lateral amygdala (LA) and basolateral amygdala (BLA) subdivisions. An increase was also seen in the hippocampal CA1 and CA3 subregions of S1 mice. No difference in mGlu7 receptor levels were seen in the central nucleus (CeA) of the amygdala, dentate gyrus (DG) of the hippocampus or prefrontal cortex. Conclusions: These data show altered mGlu7 receptor expression in key brain regions associated with fear extinction in two different inbred mouse strains which differ markedly in their fear extinction behaviour. Altered mGlu7 receptor levels may contribute to the deficit fear extinction processes seen in fear extinction in the S1 strain.en
dc.description.sponsorshipScience Foundation Ireland (Grant Numbers 07/CE/BI368 and 12/RC/2273); Austrian Science Fund (FWF SFB F4410)en
dc.description.statusPeer revieweden
dc.description.versionAccepted Versionen
dc.format.mimetypeapplication/pdfen
dc.identifier.citationO’Connor, R. M., McCafferty, C. P., Bravo, J. A., Singewald, N., Holmes, A. and Cryan, J. F. (2019) 'Increased amygdalar metabotropic glutamate receptor 7 mRNA in a genetic mouse model of impaired fear extinction', Psychopharmacology, 236, pp. 265-272. https://doi.org/10.1007/s00213-018-5031-4en
dc.identifier.doihttps://doi.org/10.1007/s00213-018-5031-4en
dc.identifier.eissn1432-2072en
dc.identifier.endpage272en
dc.identifier.issn0033-3158en
dc.identifier.journaltitlePsychopharmacologyen
dc.identifier.startpage265en
dc.identifier.urihttps://hdl.handle.net/10468/15883
dc.identifier.volume236en
dc.language.isoenen
dc.publisherSpringer Natureen
dc.rights© 2018, Springer-Verlag GmbH Germany, part of Springer Nature. This version of the paper has been accepted for publication, after peer review (when applicable) and is subject to Springer Nature’s AM terms of use, but is not the Version of Record and does not reflect post-acceptance improvements, or any corrections. The Version of Record is available online at: https://doi.org/10.1007/s00213-018-5031-4en
dc.subjectmGlu7 receptor expressionen
dc.subjectPost-traumatic stress disorderen
dc.subjectTraumaen
dc.titleIncreased amygdalar metabotropic glutamate receptor 7 mRNA in a genetic mouse model of impaired fear extinctionen
dc.typeArticle (peer-reviewed)en
oaire.citation.issue1en
oaire.citation.volume236en
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