{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,31]],"date-time":"2026-10-31T03:57:09Z","timestamp":1793419029301,"version":"4.5.0"},"reference-count":50,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2023,3,7]],"date-time":"2023-03-07T00:00:00Z","timestamp":1678147200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","award":["R01 NS091177"],"award-info":[{"award-number":["R01 NS091177"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"German Research Foundation","doi-asserted-by":"publisher","award":["EN1291\/1-1"],"award-info":[{"award-number":["EN1291\/1-1"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"German Research Foundation","doi-asserted-by":"publisher","award":["5T32HL007901-22"],"award-info":[{"award-number":["5T32HL007901-22"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000097","name":"National Center for Research Resources","doi-asserted-by":"publisher","award":["UL1 RR02758"],"award-info":[{"award-number":["UL1 RR02758"]}],"id":[{"id":"10.13039\/100000097","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000097","name":"National Center for Research Resources","doi-asserted-by":"publisher","award":["M01-RR-01032"],"award-info":[{"award-number":["M01-RR-01032"]}],"id":[{"id":"10.13039\/100000097","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2023,6,13]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Study Objectives<\/jats:title>\n                  <jats:p>There is strong evidence that sleep disturbances are an independent risk factor for the development of chronic pain conditions. The mechanisms underlying this association, however, are still not well understood. We examined the effect of experimental sleep disturbances (ESDs) on three pathways involved in pain initiation\/resolution: (1) the central pain-inhibitory pathway, (2) the cyclooxygenase (COX) pathway, and (3) the endocannabinoid (eCB) pathway.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>Twenty-four healthy participants (50% females) underwent two 19-day long in-laboratory protocols in randomized order: (1) an ESD protocol consisting of repeated nights of short and disrupted sleep with intermittent recovery sleep; and (2) a sleep control protocol consisting of nights with an 8-hour sleep opportunity. Pain inhibition (conditioned pain modulation, habituation to repeated pain), COX-2 expression at monocyte level (lipopolysaccharide [LPS]-stimulated and spontaneous), and eCBs (arachidonoylethanolamine, 2-arachidonoylglycerol, docosahexaenoylethanolamide [DHEA], eicosapentaenoylethanolamide, docosatetraenoylethanolamide) were measured every other day throughout the protocol.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>The central pain-inhibitory pathway was compromised by sleep disturbances in females, but not in males (p &amp;lt; 0.05 condition \u00d7 sex effect). The COX-2 pathway (LPS-stimulated) was activated by sleep disturbances (p &amp;lt; 0.05 condition effect), and this effect was exclusively driven by males (p &amp;lt; 0.05 condition \u00d7 sex effect). With respect to the eCB pathway, DHEA was higher (p &amp;lt; 0.05 condition effect) in the sleep disturbance compared to the control condition, without sex-differential effects on any eCBs.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>These findings suggest that central pain-inhibitory and COX mechanisms through which sleep disturbances may contribute to chronic pain risk are sex specific, implicating the need for sex-differential therapeutic targets to effectively reduce chronic pain associated with sleep disturbances in both sexes.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Clinical Trials Registration<\/jats:title>\n                  <jats:p>NCT02484742: Pain Sensitization and Habituation in a Model of Experimentally-induced Insomnia Symptoms. https:\/\/clinicaltrials.gov\/ct2\/show\/NCT02484742.<\/jats:p>\n               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USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4014-6429","authenticated-orcid":false,"given":"Rammy","family":"Dang","sequence":"additional","affiliation":[{"name":"Department of Neurology, Beth Israel Deaconess Medical Center , Boston, MA , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keeyon","family":"Olia","sequence":"additional","affiliation":[{"name":"Department of Neurology, Beth Israel Deaconess Medical Center , Boston, MA , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Victoria","family":"Molina","sequence":"additional","affiliation":[{"name":"Department of Neurology, Beth Israel Deaconess Medical Center , Boston, MA , USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Suzanne M","family":"Bertisch","sequence":"additional","affiliation":[{"name":"Harvard Medical School , Boston, MA , USA"},{"name":"Division of Sleep and Circadian Disorders, Department of 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