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Prostaglandin-mediated inhibition of serotonin signaling controls the affective component of inflammatory pain
Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences.
Linköping University, Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
Linköping University, Department of Clinical and Experimental Medicine, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.ORCID iD: 0000-0003-2245-3396
Linköping University, Department of Clinical and Experimental Medicine. Linköping University, Faculty of Medicine and Health Sciences.
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2017 (English)In: Journal of Clinical Investigation, ISSN 0021-9738, E-ISSN 1558-8238, Vol. 127, no 4, 1370-1374 p.Article in journal (Refereed) Published
Abstract [en]

Pain is fundamentally unpleasant and induces a negative affective state. The affective component of pain is mediated by circuits that are distinct from those mediating the sensory-discriminative component. Here, we have investigated the role of prostaglandins in the affective dimension of pain using a rodent pain assay based on conditioned place aversion to formalin injection, an inflammatory noxious stimulus. We found that place aversion induced by inflammatory pain depends on prostaglandin E-2 that is synthesized by cyclooxygenase 2 in neural cells. Further, mice lacking the prostaglandin E-2 receptor EP3 selectively on serotonergic cells or selectively in the area of the dorsal raphe nucleus failed to form an aversion to formalininduced pain, as did mice lacking the serotonin transporter. Chemogenetic manipulations revealed that EP3 receptor activation elicited conditioned place aversion to pain via inhibition of serotonergic neurons. In contrast to their role in inflammatory pain aversion, EP3 receptors on serotonergic cells were dispensable for acute nociceptive behaviors and for aversion induced by thermal pain or a kappa opioid receptor agonist. Collectively, our findings show that prostaglandin-mediated modulation of serotonergic transmission controls the affective component of inflammatory pain.

Place, publisher, year, edition, pages
AMER SOC CLINICAL INVESTIGATION INC , 2017. Vol. 127, no 4, 1370-1374 p.
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Neurosciences
Identifiers
URN: urn:nbn:se:liu:diva-136568DOI: 10.1172/JCI90678ISI: 000398183300026PubMedID: 28287401OAI: oai:DiVA.org:liu-136568DiVA: diva2:1090312
Note

Funding Agencies|European Research Council; Swedish Medical Research Council; Knut and Alice Wallenberg Foundation; Swedish Brain Foundation; County Council of Ostergotland; National Institute of Neurological Disorders and Stroke (NINDS)

Available from: 2017-04-24 Created: 2017-04-24 Last updated: 2017-05-21

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Singh, Anand KumarZajdel, JoannaMirrasekhian, ElaheAlmoosawi, NaderFrisch, IsabellKlawonn, AnnaJaarola, MaaritFritz, MichaelEngblom, David
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Division of Cell BiologyFaculty of Medicine and Health SciencesCenter for Social and Affective NeuroscienceDepartment of Clinical and Experimental Medicine
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