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dc.contributor.authorMoriarty, Orla
dc.contributor.authorGorman, Claire L.
dc.contributor.authorMcGowan, Fiona
dc.contributor.authorFord, Gemma K.
dc.contributor.authorRoche, Michelle
dc.contributor.authorThompson, Kerry
dc.contributor.authorDockery, Peter
dc.contributor.authorMcGuire, Brian E.
dc.contributor.authorFinn, David P.
dc.date.accessioned2019-04-01T11:19:38Z
dc.date.available2019-04-01T11:19:38Z
dc.date.issued2016-01-01
dc.identifier.citationMoriarty, Orla, Gorman Claire, L., McGowan, Fiona, Ford Gemma, K., Roche, Michelle, Thompson, Kerry, Dockery, Peter, McGuire, Brian E., Finn David, P. (2016). Impaired recognition memory and cognitive flexibility in the rat L5–L6 spinal nerve ligation model of neuropathic pain, Scandinavian Journal of Pain,10 :61-73, doi: 10.1016/j.sjpain.2015.09.008 10 :61-73.en_IE
dc.identifier.issn1877-8879
dc.identifier.urihttp://hdl.handle.net/10379/15085
dc.description.abstractBackground and aims: Although neuropathic pain is known to negatively affect cognition, the neural mechanisms involved are poorly understood. Chronic pain is associated with changes in synaptic plasticity in the brain which may impact on cognitive functioning. The aim of this study was to model neuropathic pain in mid-aged rats using spinal nerve ligation (SNL). Following establishment of allodynia and hyperalgesia, behaviour was assessed in a battery of cognitive tests. Expression of the presynaptic protein, synaptophysin, and its colocalisation with the vesicular GABA and glutamate transporters (vGAT and vGLUT, respectively), was investigated in the medial prefrontal cortex (mPFC) and hippocampus.Methods: Nine month old male Sprague Dawley rats underwent L5-L6 spinal nerve ligation or a sham procedure. Mechanical and cold allodynia and thermal hyperalgesia were assessed using von Frey, acetone and Hargreaves tests, respectively. Cognition was assessed in the novel-object recognition, air-puff passive avoidance and Morris water maze behavioural tasks. Immunohistochemistry was used to examine the expression of synaptophysin in the mPFC and CA1 region of the hippocampus and double labelling of synaptophysin and the vesicular transporters vGAT and vGlut was used to investigate the distribution of synaptophysin on GABAergic and glutamatergic neurons.Results: SNL rats displayed impaired performance in the novel-object recognition task. Passive-avoidance responding, and spatial learning and memory in the Morris water maze, were unaffected by SNL surgery. However, in the water maze reversal task, pain-related impairments were evident during training and probe trials. SNL surgery was not associated with any differences in the expression of synaptophysin or its colocalisation with vGAT or vGLUT in the mPFC or the hippocampal CA1 region.Conclusions: These results suggest that the SNL model of neuropathic pain is associated with deficits in recognition memory and cognitive flexibility, but these deficits are not associated with altered synaptophysin expression or distribution in the mPFC and CA1.Implications: Cognitive complaints are common amongst chronic pain patients. Here we modelled cognitive impairment in a well-established animal model of neuropathic pain and investigated the neural mechanisms involved. A better understanding of this phenomenon is an important prerequisite for the development of improved treatment of patients affected. (C) 2015 Scandinavian Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.en_IE
dc.description.sponsorshipThis work was supported through the National Biophotonics and Imaging Platform, Ireland, and funded by the Irish Government’s Programme for Research in Third Level Institutions, Cycle 4, Ireland’s EU Structural Funds Programmes 2007–2013. The funding agency played no part in study design; in the collection, analysis and interpretation of data; in the writing of the report; or in the decision to submit the article for publication.en_IE
dc.formatapplication/pdfen_IE
dc.language.isoenen_IE
dc.publisherDe Gruyteren_IE
dc.relation.ispartofScandinavian Journal Of Painen
dc.subjectNeuropathic painen_IE
dc.subjectSpinal nerve ligationen_IE
dc.subjectRecognition memoryen_IE
dc.subjectCognitive flexibilityen_IE
dc.subjectSynaptophysinen_IE
dc.subjectANTERIOR CINGULATE CORTEXen_IE
dc.subjectLONG-TERM POTENTIATIONen_IE
dc.subjectLOW-BACK-PAINen_IE
dc.subjectSYNAPTIC PLASTICITYen_IE
dc.subjectWORKING-MEMORYen_IE
dc.subjectINFLAMMATORY PAINen_IE
dc.subjectFIBROMYALGIA PATIENTSen_IE
dc.subjectFUNCTIONAL-CHANGESen_IE
dc.subjectPREFRONTAL CORTEXen_IE
dc.subjectCHRONIC MORPHINEen_IE
dc.titleImpaired recognition memory and cognitive flexibility in the rat L5-L6 spinal nerve ligation model of neuropathic painen_IE
dc.typeArticleen_IE
dc.date.updated2019-03-28T05:19:07Z
dc.identifier.doi10.1016/j.sjpain.2015.09.008
dc.local.publishedsourcehttps://doi.org/10.1016/j.sjpain.2015.09.008en_IE
dc.description.peer-reviewedpeer-reviewed
dc.contributor.funderNational Biophotonics and Imaging Platform, Irelanden_IE
dc.contributor.funderEU Structural Fundsen_IE
dc.internal.rssid11254754
dc.local.contactDavid Finn, Dept. Of Pharmacology &, Therapeutics, Nui, Galway. 5280 Email: david.finn@nuigalway.ie
dc.local.copyrightcheckedYes
dc.local.versionACCEPTED
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