NAPE-PLD regulates specific baseline affective behaviors but is dispensable for inflammatory hyperalgesia

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dc.contributor.authorChen, Ireneen
dc.contributor.authorMurdaugh, Laura B.en
dc.contributor.authorMiliano, Cristinaen
dc.contributor.authorDong, Yuyangen
dc.contributor.authorGregus, Ann M.en
dc.contributor.authorBuczynski, Matthew W.en
dc.date.accessioned2024-03-06T20:42:32Zen
dc.date.available2024-03-06T20:42:32Zen
dc.date.issued2023-06-14en
dc.description.abstractN-acyl-ethanolamine (NAEs) serve as key endogenous lipid mediators as revealed by manipulation of fatty acid amide hydrolase (FAAH), the primary enzyme responsible for metabolizing NAEs. Preclinical studies focused on FAAH or NAE receptors indicate an important role for NAE signaling in nociception and affective behaviors. However, there is limited information on the role of NAE biosynthesis in these same behavioral paradigms. Biosynthesis of NAEs has been attributed largely to the enzyme N-acylphosphatidylethanolamine Phospholipase D (NAPE-PLD), one of three pathways capable of producing these bioactive lipids in the brain. In this report, we demonstrate that Nape-pld knockout (KO) mice displayed reduced sucrose preference and consumption, but other baseline anxiety-like or depression-like behaviors were unaltered. Additionally, we observed sex-dependent responses in thermal nociception and other baseline measures in wildtype (WT) mice that were absent in Nape-pld KO mice. In the Complete Freund's Adjuvant (CFA) model of inflammatory arthritis, WT mice exhibited sex-dependent changes in paw edema that were lost in Nape-pld KO mice. However, there was no effect of Nape-pld deletion on arthritic pain-like behaviors (grip force deficit and tactile allodynia) in either sex, indicating that while NAPE-PLD may alter local inflammation, it does not contribute to pain-like behaviors associated with inflammatory arthritis. Collectively, these findings indicate that chronic and systemic NAPE-PLD inactivation will likely be well-tolerated, warranting further pharmacological evaluation of this target in other disease indications.en
dc.description.versionPublished versionen
dc.format.mimetypeapplication/pdfen
dc.identifier100135 (Article number)en
dc.identifier.doihttps://doi.org/10.1016/j.ynpai.2023.100135en
dc.identifier.eissn2452-073Xen
dc.identifier.issn2452-073Xen
dc.identifier.orcidBuczynski, Matthew [0000-0001-5931-7107]en
dc.identifier.otherPMC10719515en
dc.identifier.otherS2452-073X(23)00022-3 (PII)en
dc.identifier.pmid38099275en
dc.identifier.urihttps://hdl.handle.net/10919/118293en
dc.identifier.volume14en
dc.language.isoenen
dc.publisherElsevieren
dc.relation.urihttps://www.ncbi.nlm.nih.gov/pubmed/38099275en
dc.rightsCreative Commons Attribution-NonCommercial-NoDerivatives 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en
dc.subjectArthritisen
dc.subjectDepressionen
dc.subjectEndocannabinoidsen
dc.subjectHyperalgesiaen
dc.subjectLipidsen
dc.subjectSex differenceen
dc.titleNAPE-PLD regulates specific baseline affective behaviors but is dispensable for inflammatory hyperalgesiaen
dc.title.serialNeurobiology of Painen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten
dc.type.otherJournal Articleen
dcterms.dateAccepted2023-06-08en
pubs.organisational-group/Virginia Techen
pubs.organisational-group/Virginia Tech/Scienceen
pubs.organisational-group/Virginia Tech/Faculty of Health Sciencesen
pubs.organisational-group/Virginia Tech/All T&R Facultyen
pubs.organisational-group/Virginia Tech/Science/COS T&R Facultyen
pubs.organisational-group/Virginia Tech/Science/School of Neuroscienceen

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