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dc.contributor.authorRea, Kieran
dc.contributor.authorOlango, Weredeselam M.
dc.contributor.authorHarhen, Brendan
dc.contributor.authorKerr, Daniel M.
dc.contributor.authorGalligan, Rachel
dc.contributor.authorFitzgerald, Sean
dc.contributor.authorMoore, Maeve
dc.contributor.authorRoche, Michelle
dc.contributor.authorFinn, David P.
dc.date.accessioned2019-08-30T08:54:02Z
dc.date.available2019-08-30T08:54:02Z
dc.date.issued2012-12-31
dc.identifier.citationRea K, Olango WM, Harhen B, Kerr DM, Galligan R, Fitzgerald S, Moore M,Roche M, Finn, DP (2013). Evidence for a role ofGABAergic and glutamatergic signalingin thebasolateral amygdala in endocannabinoid-mediated fear-conditioned analgesiainRats. Pain, 154(4),576 85. DOI: https://doi.org/10.1016/j.pain.2012.12.021en_IE
dc.identifier.issn1872-6623
dc.identifier.urihttp://hdl.handle.net/10379/15364
dc.description.abstractThe basolateral amygdala (BLA) is a key substrate facilitating the expression of fear-conditioned analgesia (FCA). However, the neurochemical mechanisms in the BLA which mediate this potent suppression of pain responding during fear remain unknown. The present study investigated the role of cannabinoid(1) (CB1) receptors and interactions with GABAergic (GABA(A) receptor) and glutamatergic (metabotropic glutamate receptor type 5; mGluR5) signalling in the BLA in formalin-evoked nociceptive behaviour and FCA in rats. Reexposure to a context previously paired with foot shock significantly reduced formalin-evoked nociceptive behaviour. Systemic or intra-BLA microinjection of the CB1 receptor antagonist/inverse agonist AM251 prevented this expression of FCA, while injection of AM251 into the central nucleus of the amygdala did not. The suppression of FCA by systemic AM251 administration was partially attenuated by intra-BLA administration of either the GABA(A) receptor antagonist bicuculline or the mGluR5 antagonist 2-methyl-6-(phenylethynyl) pyridine, (MPEP). Bilateral microinjection of MPEP, but not bicuculline, alone into the BLA enhanced formalin-evoked nociceptive behaviour. Postmortem analyses revealed that FCA was associated with a significant increase in tissue levels of anandamide in the BLA side contralateral to intraplantar formalin injection. In addition, fear-conditioned rats exhibited a robust formalin-induced increase in levels of 2-arachidonyl glycerol and N-palmitoylethanolamide in the ipsilateral and contralateral BLA, respectively. These data suggest that CB1 receptors in the BLA facilitate the expression of FCA, through a mechanism which is likely to involve the modulation of GABAergic and glutamatergic signalling. (c) 2012 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.en_IE
dc.language.isoenen_IE
dc.publisherElsevieren_IE
dc.relation.ispartofPainen
dc.subjectAM251en_IE
dc.subjectAmygdalaen_IE
dc.subjectBicucullineen_IE
dc.subjectCannabinoid(1) (CB1) receptoren_IE
dc.subjectMPEPen_IE
dc.subjectPainen_IE
dc.subjectSTRESS-INDUCED ANALGESIAen_IE
dc.subjectFATTY-ACID AMIDEen_IE
dc.subjectCANNABINOID RECEPTOR CB1en_IE
dc.subjectVANILLOID TYPE-1 RECEPTORSen_IE
dc.subjectLONG-TERM POTENTIATIONen_IE
dc.subjectCENTRAL-NERVOUS-SYSTEMen_IE
dc.subjectPERIAQUEDUCTAL GRAYen_IE
dc.subjectHEMISPHERIC LATERALIZATIONen_IE
dc.subjectINFLAMMATORY PAINen_IE
dc.subjectFOS EXPRESSIONen_IE
dc.titleEvidence for a role of GABAergic and glutamatergic signalling in the basolateral amygdala in endocannabinoid-mediated fear-conditioned analgesia in ratsen_IE
dc.typeArticleen_IE
dc.date.updated2016-04-22T15:40:50Z
dc.identifier.doi10.1016/j.pain.2012.12.021
dc.local.publishedsourcehttps://doi.org/10.1016/j.pain.2012.12.021en_IE
dc.description.peer-reviewedpeer-reviewed
dc.internal.rssid4339999
dc.local.contactMichelle Roche, Dept Of Physiology, Nui Galway. 5427 Email: michelle.roche@nuigalway.ie
dc.local.copyrightcheckedYes
dc.local.versionPUBLISHED
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