Pain-Related Depression of the Mesolimbic Dopamine System in Rats: Expression, Blockade by Analgesics, and Role of Endogenous κ-opioids
Pain is often associated with depression of behavior and mood, and relief of pain-related depression is a common goal of treatment. This study tested the hypothesis that pain-related behavioral depression is mediated by activation of endogenous κ-opioid systems and subsequent depression of mesolimbi...
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description | Pain is often associated with depression of behavior and mood, and relief of pain-related depression is a common goal of treatment. This study tested the hypothesis that pain-related behavioral depression is mediated by activation of endogenous κ-opioid systems and subsequent depression of mesolimbic dopamine release. Adult male Sprague-Dawley rats were implanted with electrodes targeting the medial forebrain bundle (for behavior studies of intracranial self-stimulation (ICSS)) or with cannulae for microdialysis measures of nucleus accumbens dopamine (NAc DA). Changes in ICSS and NAc DA were examined after treatment with a visceral noxious stimulus (intraperitoneal injection of dilute lactic acid) or an exogenous κ-agonist (U69593). Additional studies examined the sensitivity of acid and U69593 effects to blockade by two analgesics (the nonsteroidal antiinflammatory drug ketoprofen and the μ-opioid agonist morphine) or by the κ-antagonist norbinaltorphimine (norBNI). The effects of acid were also examined on mRNA expression for prodynorphin (PDYN) and κ-opioid receptors (KORs) in mesocorticolimbic brain regions. Both acid and U69593 depressed ICSS and extracellular levels of NAc DA. Pain-related acid effects were blocked by ketoprofen and morphine but not by norBNI. The U69593 effects were blocked by norBNI but not by ketoprofen, and were only attenuated by morphine. Acid did not significantly alter PDYN or KOR in NAc, but it produced a delayed increase in PDYN in prefrontal cortex. These results support a key role for the mesolimbic DA system, but a more nuanced role for endogenous κ-opioid systems, in mediating acute pain-related behavioral depression in rats. |
doi_str_mv | 10.1038/npp.2013.236 |
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Scott ; KEJUN CHENG ; RICE, Kenner C ; CARLEZON, William A ; BANKS, Matthew L ; NEGUS, S. Stevens</creator><creatorcontrib>LEITL, Michael D ; ONVANI, Sara ; BOWERS, M. Scott ; KEJUN CHENG ; RICE, Kenner C ; CARLEZON, William A ; BANKS, Matthew L ; NEGUS, S. Stevens</creatorcontrib><description>Pain is often associated with depression of behavior and mood, and relief of pain-related depression is a common goal of treatment. This study tested the hypothesis that pain-related behavioral depression is mediated by activation of endogenous κ-opioid systems and subsequent depression of mesolimbic dopamine release. Adult male Sprague-Dawley rats were implanted with electrodes targeting the medial forebrain bundle (for behavior studies of intracranial self-stimulation (ICSS)) or with cannulae for microdialysis measures of nucleus accumbens dopamine (NAc DA). Changes in ICSS and NAc DA were examined after treatment with a visceral noxious stimulus (intraperitoneal injection of dilute lactic acid) or an exogenous κ-agonist (U69593). Additional studies examined the sensitivity of acid and U69593 effects to blockade by two analgesics (the nonsteroidal antiinflammatory drug ketoprofen and the μ-opioid agonist morphine) or by the κ-antagonist norbinaltorphimine (norBNI). The effects of acid were also examined on mRNA expression for prodynorphin (PDYN) and κ-opioid receptors (KORs) in mesocorticolimbic brain regions. Both acid and U69593 depressed ICSS and extracellular levels of NAc DA. Pain-related acid effects were blocked by ketoprofen and morphine but not by norBNI. The U69593 effects were blocked by norBNI but not by ketoprofen, and were only attenuated by morphine. Acid did not significantly alter PDYN or KOR in NAc, but it produced a delayed increase in PDYN in prefrontal cortex. These results support a key role for the mesolimbic DA system, but a more nuanced role for endogenous κ-opioid systems, in mediating acute pain-related behavioral depression in rats.</description><identifier>ISSN: 0893-133X</identifier><identifier>EISSN: 1740-634X</identifier><identifier>DOI: 10.1038/npp.2013.236</identifier><identifier>PMID: 24008352</identifier><identifier>CODEN: NEROEW</identifier><language>eng</language><publisher>Basingstoke: Nature Publishing Group</publisher><subject>Adult and adolescent clinical studies ; Analgesics ; Analgesics, Opioid - pharmacology ; Animals ; Benzeneacetamides - pharmacology ; Biological and medical sciences ; Depression ; Depression - etiology ; Depression - metabolism ; Depression - pathology ; Disease Models, Animal ; Dopamine - metabolism ; Gene Expression Regulation - drug effects ; Ketoprofen - pharmacology ; Lactic Acid - pharmacology ; Male ; Medial Forebrain Bundle - drug effects ; Medial Forebrain Bundle - physiology ; Medical sciences ; Mood disorders ; Morphine - pharmacology ; Naltrexone - analogs & derivatives ; Naltrexone - pharmacology ; Narcotic Antagonists - pharmacology ; Nucleus Accumbens - drug effects ; Nucleus Accumbens - metabolism ; Original ; Pain - complications ; Pain - drug therapy ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Pyrrolidines - pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Opioid, kappa - genetics ; Receptors, Opioid, kappa - metabolism ; Self Stimulation ; Time Factors</subject><ispartof>Neuropsychopharmacology (New York, N.Y.), 2014-02, Vol.39 (3), p.614-624</ispartof><rights>2015 INIST-CNRS</rights><rights>Copyright © 2014 American College of Neuropsychopharmacology 2014 American College of Neuropsychopharmacology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c447t-1da60fb76f9103b21e3c3a252f340bc603826fe974acedccd5a67912fd5646c33</citedby><cites>FETCH-LOGICAL-c447t-1da60fb76f9103b21e3c3a252f340bc603826fe974acedccd5a67912fd5646c33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3895239/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3895239/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28283133$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24008352$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>LEITL, Michael D</creatorcontrib><creatorcontrib>ONVANI, Sara</creatorcontrib><creatorcontrib>BOWERS, M. Scott</creatorcontrib><creatorcontrib>KEJUN CHENG</creatorcontrib><creatorcontrib>RICE, Kenner C</creatorcontrib><creatorcontrib>CARLEZON, William A</creatorcontrib><creatorcontrib>BANKS, Matthew L</creatorcontrib><creatorcontrib>NEGUS, S. Stevens</creatorcontrib><title>Pain-Related Depression of the Mesolimbic Dopamine System in Rats: Expression, Blockade by Analgesics, and Role of Endogenous κ-opioids</title><title>Neuropsychopharmacology (New York, N.Y.)</title><addtitle>Neuropsychopharmacology</addtitle><description>Pain is often associated with depression of behavior and mood, and relief of pain-related depression is a common goal of treatment. This study tested the hypothesis that pain-related behavioral depression is mediated by activation of endogenous κ-opioid systems and subsequent depression of mesolimbic dopamine release. Adult male Sprague-Dawley rats were implanted with electrodes targeting the medial forebrain bundle (for behavior studies of intracranial self-stimulation (ICSS)) or with cannulae for microdialysis measures of nucleus accumbens dopamine (NAc DA). Changes in ICSS and NAc DA were examined after treatment with a visceral noxious stimulus (intraperitoneal injection of dilute lactic acid) or an exogenous κ-agonist (U69593). Additional studies examined the sensitivity of acid and U69593 effects to blockade by two analgesics (the nonsteroidal antiinflammatory drug ketoprofen and the μ-opioid agonist morphine) or by the κ-antagonist norbinaltorphimine (norBNI). The effects of acid were also examined on mRNA expression for prodynorphin (PDYN) and κ-opioid receptors (KORs) in mesocorticolimbic brain regions. Both acid and U69593 depressed ICSS and extracellular levels of NAc DA. Pain-related acid effects were blocked by ketoprofen and morphine but not by norBNI. The U69593 effects were blocked by norBNI but not by ketoprofen, and were only attenuated by morphine. Acid did not significantly alter PDYN or KOR in NAc, but it produced a delayed increase in PDYN in prefrontal cortex. These results support a key role for the mesolimbic DA system, but a more nuanced role for endogenous κ-opioid systems, in mediating acute pain-related behavioral depression in rats.</description><subject>Adult and adolescent clinical studies</subject><subject>Analgesics</subject><subject>Analgesics, Opioid - pharmacology</subject><subject>Animals</subject><subject>Benzeneacetamides - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Depression</subject><subject>Depression - etiology</subject><subject>Depression - metabolism</subject><subject>Depression - pathology</subject><subject>Disease Models, Animal</subject><subject>Dopamine - metabolism</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Ketoprofen - pharmacology</subject><subject>Lactic Acid - pharmacology</subject><subject>Male</subject><subject>Medial Forebrain Bundle - drug effects</subject><subject>Medial Forebrain Bundle - physiology</subject><subject>Medical sciences</subject><subject>Mood disorders</subject><subject>Morphine - pharmacology</subject><subject>Naltrexone - analogs & derivatives</subject><subject>Naltrexone - pharmacology</subject><subject>Narcotic Antagonists - pharmacology</subject><subject>Nucleus Accumbens - drug effects</subject><subject>Nucleus Accumbens - metabolism</subject><subject>Original</subject><subject>Pain - complications</subject><subject>Pain - drug therapy</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Pyrrolidines - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Opioid, kappa - genetics</subject><subject>Receptors, Opioid, kappa - metabolism</subject><subject>Self Stimulation</subject><subject>Time Factors</subject><issn>0893-133X</issn><issn>1740-634X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkc1u1DAURi0EokNhxxp5g8RiMvVP4iQsKpV2oJWKQANI3Vk3zs3U4NghziDmDXimPgTPhEedFljdhY8_38-HkOecLTiT1ZEfhoVgXC6EVA_IjJc5y5TMrx6SGatqmXEprw7Ikxi_MsaLUlWPyYHIGatkIWbk10ewPluhgwlbeobDiDHa4Gno6HSN9D3G4GzfWEPPwgC99Ug_beOEPbWermCKr-ny592tOX3jgvkGLdJmS088uDVGa-Kcgm_pKjjc5S59G9bowybS3zdZGGywbXxKHnXgIj7bz0Py5e3y8-l5dvnh3cXpyWVm8rycMt6CYl1Tqq5O7RvBURoJohCdzFljVPoRoTqsyxwMtsa0Baiy5qJrC5UrI-UhOb7NHTZNnwj00whOD6PtYdzqAFb_f-LttV6HH1pWdSFknQJe7QPG8H2DcdK9jQadA4-pkuZ5raqqVGqHzm9RM4YYR-zun-FM7-TpJE_v5OkkL-Ev_l3tHr6zlYCXewCiAdeN4I2Nf7lKVDLpln8AkWmlmw</recordid><startdate>20140201</startdate><enddate>20140201</enddate><creator>LEITL, Michael D</creator><creator>ONVANI, Sara</creator><creator>BOWERS, M. 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Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Pyrrolidines - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Opioid, kappa - genetics</topic><topic>Receptors, Opioid, kappa - metabolism</topic><topic>Self Stimulation</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>LEITL, Michael D</creatorcontrib><creatorcontrib>ONVANI, Sara</creatorcontrib><creatorcontrib>BOWERS, M. Scott</creatorcontrib><creatorcontrib>KEJUN CHENG</creatorcontrib><creatorcontrib>RICE, Kenner C</creatorcontrib><creatorcontrib>CARLEZON, William A</creatorcontrib><creatorcontrib>BANKS, Matthew L</creatorcontrib><creatorcontrib>NEGUS, S. 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Stevens</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pain-Related Depression of the Mesolimbic Dopamine System in Rats: Expression, Blockade by Analgesics, and Role of Endogenous κ-opioids</atitle><jtitle>Neuropsychopharmacology (New York, N.Y.)</jtitle><addtitle>Neuropsychopharmacology</addtitle><date>2014-02-01</date><risdate>2014</risdate><volume>39</volume><issue>3</issue><spage>614</spage><epage>624</epage><pages>614-624</pages><issn>0893-133X</issn><eissn>1740-634X</eissn><coden>NEROEW</coden><abstract>Pain is often associated with depression of behavior and mood, and relief of pain-related depression is a common goal of treatment. This study tested the hypothesis that pain-related behavioral depression is mediated by activation of endogenous κ-opioid systems and subsequent depression of mesolimbic dopamine release. Adult male Sprague-Dawley rats were implanted with electrodes targeting the medial forebrain bundle (for behavior studies of intracranial self-stimulation (ICSS)) or with cannulae for microdialysis measures of nucleus accumbens dopamine (NAc DA). Changes in ICSS and NAc DA were examined after treatment with a visceral noxious stimulus (intraperitoneal injection of dilute lactic acid) or an exogenous κ-agonist (U69593). Additional studies examined the sensitivity of acid and U69593 effects to blockade by two analgesics (the nonsteroidal antiinflammatory drug ketoprofen and the μ-opioid agonist morphine) or by the κ-antagonist norbinaltorphimine (norBNI). The effects of acid were also examined on mRNA expression for prodynorphin (PDYN) and κ-opioid receptors (KORs) in mesocorticolimbic brain regions. Both acid and U69593 depressed ICSS and extracellular levels of NAc DA. Pain-related acid effects were blocked by ketoprofen and morphine but not by norBNI. The U69593 effects were blocked by norBNI but not by ketoprofen, and were only attenuated by morphine. Acid did not significantly alter PDYN or KOR in NAc, but it produced a delayed increase in PDYN in prefrontal cortex. These results support a key role for the mesolimbic DA system, but a more nuanced role for endogenous κ-opioid systems, in mediating acute pain-related behavioral depression in rats.</abstract><cop>Basingstoke</cop><pub>Nature Publishing Group</pub><pmid>24008352</pmid><doi>10.1038/npp.2013.236</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adult and adolescent clinical studies Analgesics Analgesics, Opioid - pharmacology Animals Benzeneacetamides - pharmacology Biological and medical sciences Depression Depression - etiology Depression - metabolism Depression - pathology Disease Models, Animal Dopamine - metabolism Gene Expression Regulation - drug effects Ketoprofen - pharmacology Lactic Acid - pharmacology Male Medial Forebrain Bundle - drug effects Medial Forebrain Bundle - physiology Medical sciences Mood disorders Morphine - pharmacology Naltrexone - analogs & derivatives Naltrexone - pharmacology Narcotic Antagonists - pharmacology Nucleus Accumbens - drug effects Nucleus Accumbens - metabolism Original Pain - complications Pain - drug therapy Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Pyrrolidines - pharmacology Rats Rats, Sprague-Dawley Receptors, Opioid, kappa - genetics Receptors, Opioid, kappa - metabolism Self Stimulation Time Factors |
title | Pain-Related Depression of the Mesolimbic Dopamine System in Rats: Expression, Blockade by Analgesics, and Role of Endogenous κ-opioids |
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