Muldoon, Pretal P.AiSharari, ShakirCarroll, F. IvyNegus, S. StevensDamaj, M. Imad2022-10-262022-10-262016-03Bağdaş, D. vd. (2016). "Expression and pharmacological modulation of visceral pain-induced conditioned place aversion in mice". Neuropharmacology, 102, 236-243.0028-39081873-7064https://doi.org/10.1016/j.neuropharm.2015.11.024https://www.sciencedirect.com/science/article/pii/S002839081530188Xhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5574195/http://hdl.handle.net/11452/29218Pain encompasses both a sensory as well as an affective dimension and these are differentially processed in the brain and periphery. It is therefore important to develop animal models to reflect the non-reflexive assays in pain. In this study, we compared effects of the mu opioid receptor agonist morphine, the nonsteroidal anti-inflammatory drug ketoprofen and the kappa receptor opioid agonist U50,488H and antagonist JDTic on acetic acid-induced stretching and acetic acid-induced aversion in the condition place aversion (CPA) test in male ICR mice. Intraperitoneal administration of acetic acid (0.32-1%) was equipotent in stimulating stretching and CPA. Ketoprofen, morphine and U50,488H all inhibited the acid induced stretching. Ketoprofen and morphine also blocked the acid-induced CPA but U50,488H failed to do so. The reversal ability of ketoprofen and morphine on acid-induced CPA is unique to pain-stimulated place aversion since these drugs failed to reduce non-noxious LiCl-induced CPA. Overall, this study characterized and validated a preclinical mouse model of pain-related aversive behavior that can be used to assess genetic and biological mechanisms of pain as well as improving the predictive validity of preclinical studies on candidate analgesics.eninfo:eu-repo/semantics/openAccessNeurosciences & neurologyPharmacology & pharmacyAcetic acidConditioned place aversionMicePainAnalgesicsNegative affective componentAnimal-modelsPreclinical assaysAnalgesic efficacyStria terminalisBed nucleusMorphineAmygdalaActivationDepression3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-IsomerAnalgesics, opioidAnimalsAnti-inflammatory agents, non-steroidalAvoidance learningBehavior, animalKetoprofenMaleMiceMice, inbred ICRMorphinePiperidinesReceptors, opioid, kappaReceptors, opioid, muTetrahydroisoquinolinesVisceral painArticle0003689504000222-s2.0-8494845529523624310226639043NeurosciencesPharmacology & pharmacyGrimace Scale; Buprenorphine; Animals3,4 dichloro n methyl n [2 (1 pyrrolidinyl)cyclohexyl]benzeneacetamide methanesulfonateAcetic acidKetoprofenLithium chlorideMorphine3,4 dichloro n methyl n [2 (1 pyrrolidinyl)cyclohexyl]benzeneacetamide7-hydroxy-N-(1-((4-(3-hydroxyphenyl)-3,4-dimethyl-1-piperidinyl)methyl)-2-methylpropyl)-1,2,3,4-tetrahydro-3-isoquinolinecarboxamideKappa opiate receptorKetoprofenMorphineMu opiate receptorNarcotic analgesic agentNonsteroid antiinflammatory agentPiperidine derivativeTetrahydroisoquinoline derivativeAdultAnimal experimentAnimal modelArticleAversionConditioned place aversionControlled studyDrug effectDrug potencyInstitute for cancer research mouseMaleMouseNonhumanPharmacological blockingPriority journalStretchingVisceral painAgonistsAnimalAnimal behaviorAntagonists and inhibitorsAvoidance behaviorDrug effectsPathophysiologyPhysiologyVisceral pain