The role of the neurokinin-1 receptor in stress-induced reinstatement of alcohol and cocaine seeking
Neurokinin-1 receptors (NK1Rs) have been shown to mediate alcohol and opiate, but not cocaine reward in rodents. We recently reported that NK1R antagonism also blocks stress-induced reinstatement of alcohol seeking in rats, but it is presently unknown whether these antirelapse properties extend to o...
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| Veröffentlicht in: | Neuropsychopharmacology (New York, N.Y.) N.Y.), 2014-04, Vol.39 (5), p.1093-1101 |
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| creator | Schank, Jesse R King, Courtney E Sun, Hui Cheng, Kejun Rice, Kenner C Heilig, Markus Weinshenker, David Schroeder, Jason P |
| description | Neurokinin-1 receptors (NK1Rs) have been shown to mediate alcohol and opiate, but not cocaine reward in rodents. We recently reported that NK1R antagonism also blocks stress-induced reinstatement of alcohol seeking in rats, but it is presently unknown whether these antirelapse properties extend to other drug classes. Although some work has suggested that intracranial substance P (SP) infusion reinstates cocaine seeking following extinction, no studies have indicated a direct role for the NK1R in reinstatement of cocaine seeking. Here, we explored the effect of the NK1R antagonist L822429 on yohimbine-induced reinstatement of alcohol or cocaine seeking in Long-Evans rats. Consistent with our previous findings with footshock-induced reinstatement of alcohol seeking in Wistar rats, we found that L822429 attenuates yohimbine-induced reinstatement of alcohol seeking, but does not affect baseline alcohol self-administration. We observed a similar suppression of yohimbine-induced reinstatement of cocaine seeking by L822429, and found that Long-Evans rats exhibit greater sensitivity to NK1R antagonism than Wistar rats. Accordingly, Long-Evans rats exhibit differences in the expression of NK1Rs in some subcortical brain regions. Combined, our findings suggest that while NK1R antagonism differentially influences alcohol- and cocaine-related behavior, this receptor mediates stress-induced seeking of both drugs. |
| doi_str_mv | 10.1038/npp.2013.309 |
| format | Article |
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We recently reported that NK1R antagonism also blocks stress-induced reinstatement of alcohol seeking in rats, but it is presently unknown whether these antirelapse properties extend to other drug classes. Although some work has suggested that intracranial substance P (SP) infusion reinstates cocaine seeking following extinction, no studies have indicated a direct role for the NK1R in reinstatement of cocaine seeking. Here, we explored the effect of the NK1R antagonist L822429 on yohimbine-induced reinstatement of alcohol or cocaine seeking in Long-Evans rats. Consistent with our previous findings with footshock-induced reinstatement of alcohol seeking in Wistar rats, we found that L822429 attenuates yohimbine-induced reinstatement of alcohol seeking, but does not affect baseline alcohol self-administration. We observed a similar suppression of yohimbine-induced reinstatement of cocaine seeking by L822429, and found that Long-Evans rats exhibit greater sensitivity to NK1R antagonism than Wistar rats. Accordingly, Long-Evans rats exhibit differences in the expression of NK1Rs in some subcortical brain regions. Combined, our findings suggest that while NK1R antagonism differentially influences alcohol- and cocaine-related behavior, this receptor mediates stress-induced seeking of both drugs.</description><identifier>ISSN: 0893-133X</identifier><identifier>EISSN: 1740-634X</identifier><identifier>DOI: 10.1038/npp.2013.309</identifier><identifier>PMID: 24173499</identifier><identifier>CODEN: NEROEW</identifier><language>eng</language><publisher>England: Nature Publishing Group</publisher><subject>Adrenergic alpha-2 Receptor Antagonists - pharmacology ; Alcohol-Related Disorders - drug therapy ; Alcohol-Related Disorders - etiology ; Alcohol-Related Disorders - metabolism ; Alcoholism ; Animals ; Behavior, Addictive - chemically induced ; Behavior, Addictive - drug therapy ; Behavior, Addictive - etiology ; Behavior, Addictive - metabolism ; Brain ; Brain - metabolism ; Central Nervous System Depressants - administration & dosage ; Central Nervous System Depressants - pharmacology ; Cocaine ; Cocaine - administration & dosage ; Cocaine - pharmacology ; Cocaine-Related Disorders - drug therapy ; Cocaine-Related Disorders - etiology ; Cocaine-Related Disorders - metabolism ; Dopamine Uptake Inhibitors - administration & dosage ; Dopamine Uptake Inhibitors - pharmacology ; Ethanol - administration & dosage ; Ethanol - pharmacology ; Extinction ; Laboratory animals ; Male ; Narcotics ; Neurokinin-1 Receptor Antagonists - pharmacology ; Original ; Piperidines - pharmacology ; Rats ; Rats, Long-Evans ; Rats, Wistar ; Receptors, Neurokinin-1 - metabolism ; Recurrence ; Saccharin - administration & dosage ; Species Specificity ; Stress, Psychological - chemically induced ; Stress, Psychological - complications ; Stress, Psychological - metabolism ; Yohimbine - pharmacology</subject><ispartof>Neuropsychopharmacology (New York, N.Y.), 2014-04, Vol.39 (5), p.1093-1101</ispartof><rights>Copyright Nature Publishing Group Apr 2014</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-c2949-60f55a48c7832aed975a4735f7634ccfbe60d6480677229d6c25af49a15329f63</citedby><cites>FETCH-LOGICAL-c2949-60f55a48c7832aed975a4735f7634ccfbe60d6480677229d6c25af49a15329f63</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/PMC3957103/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3957103/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24173499$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schank, Jesse R</creatorcontrib><creatorcontrib>King, Courtney E</creatorcontrib><creatorcontrib>Sun, Hui</creatorcontrib><creatorcontrib>Cheng, Kejun</creatorcontrib><creatorcontrib>Rice, Kenner C</creatorcontrib><creatorcontrib>Heilig, Markus</creatorcontrib><creatorcontrib>Weinshenker, David</creatorcontrib><creatorcontrib>Schroeder, Jason P</creatorcontrib><title>The role of the neurokinin-1 receptor in stress-induced reinstatement of alcohol and cocaine seeking</title><title>Neuropsychopharmacology (New York, N.Y.)</title><addtitle>Neuropsychopharmacology</addtitle><description>Neurokinin-1 receptors (NK1Rs) have been shown to mediate alcohol and opiate, but not cocaine reward in rodents. We recently reported that NK1R antagonism also blocks stress-induced reinstatement of alcohol seeking in rats, but it is presently unknown whether these antirelapse properties extend to other drug classes. Although some work has suggested that intracranial substance P (SP) infusion reinstates cocaine seeking following extinction, no studies have indicated a direct role for the NK1R in reinstatement of cocaine seeking. Here, we explored the effect of the NK1R antagonist L822429 on yohimbine-induced reinstatement of alcohol or cocaine seeking in Long-Evans rats. Consistent with our previous findings with footshock-induced reinstatement of alcohol seeking in Wistar rats, we found that L822429 attenuates yohimbine-induced reinstatement of alcohol seeking, but does not affect baseline alcohol self-administration. We observed a similar suppression of yohimbine-induced reinstatement of cocaine seeking by L822429, and found that Long-Evans rats exhibit greater sensitivity to NK1R antagonism than Wistar rats. Accordingly, Long-Evans rats exhibit differences in the expression of NK1Rs in some subcortical brain regions. Combined, our findings suggest that while NK1R antagonism differentially influences alcohol- and cocaine-related behavior, this receptor mediates stress-induced seeking of both drugs.</description><subject>Adrenergic alpha-2 Receptor Antagonists - pharmacology</subject><subject>Alcohol-Related Disorders - drug therapy</subject><subject>Alcohol-Related Disorders - etiology</subject><subject>Alcohol-Related Disorders - metabolism</subject><subject>Alcoholism</subject><subject>Animals</subject><subject>Behavior, Addictive - chemically induced</subject><subject>Behavior, Addictive - drug therapy</subject><subject>Behavior, Addictive - etiology</subject><subject>Behavior, Addictive - metabolism</subject><subject>Brain</subject><subject>Brain - metabolism</subject><subject>Central Nervous System Depressants - administration & dosage</subject><subject>Central Nervous System Depressants - pharmacology</subject><subject>Cocaine</subject><subject>Cocaine - administration & dosage</subject><subject>Cocaine - 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administration & dosage</topic><topic>Ethanol - pharmacology</topic><topic>Extinction</topic><topic>Laboratory animals</topic><topic>Male</topic><topic>Narcotics</topic><topic>Neurokinin-1 Receptor Antagonists - pharmacology</topic><topic>Original</topic><topic>Piperidines - pharmacology</topic><topic>Rats</topic><topic>Rats, Long-Evans</topic><topic>Rats, Wistar</topic><topic>Receptors, Neurokinin-1 - metabolism</topic><topic>Recurrence</topic><topic>Saccharin - administration & dosage</topic><topic>Species Specificity</topic><topic>Stress, Psychological - chemically induced</topic><topic>Stress, Psychological - complications</topic><topic>Stress, Psychological - metabolism</topic><topic>Yohimbine - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schank, Jesse R</creatorcontrib><creatorcontrib>King, Courtney E</creatorcontrib><creatorcontrib>Sun, Hui</creatorcontrib><creatorcontrib>Cheng, Kejun</creatorcontrib><creatorcontrib>Rice, Kenner C</creatorcontrib><creatorcontrib>Heilig, Markus</creatorcontrib><creatorcontrib>Weinshenker, David</creatorcontrib><creatorcontrib>Schroeder, Jason P</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Neuropsychopharmacology (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schank, Jesse R</au><au>King, Courtney E</au><au>Sun, Hui</au><au>Cheng, Kejun</au><au>Rice, Kenner C</au><au>Heilig, Markus</au><au>Weinshenker, David</au><au>Schroeder, Jason P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The role of the neurokinin-1 receptor in stress-induced reinstatement of alcohol and cocaine seeking</atitle><jtitle>Neuropsychopharmacology (New York, N.Y.)</jtitle><addtitle>Neuropsychopharmacology</addtitle><date>2014-04</date><risdate>2014</risdate><volume>39</volume><issue>5</issue><spage>1093</spage><epage>1101</epage><pages>1093-1101</pages><issn>0893-133X</issn><eissn>1740-634X</eissn><coden>NEROEW</coden><abstract>Neurokinin-1 receptors (NK1Rs) have been shown to mediate alcohol and opiate, but not cocaine reward in rodents. We recently reported that NK1R antagonism also blocks stress-induced reinstatement of alcohol seeking in rats, but it is presently unknown whether these antirelapse properties extend to other drug classes. Although some work has suggested that intracranial substance P (SP) infusion reinstates cocaine seeking following extinction, no studies have indicated a direct role for the NK1R in reinstatement of cocaine seeking. Here, we explored the effect of the NK1R antagonist L822429 on yohimbine-induced reinstatement of alcohol or cocaine seeking in Long-Evans rats. Consistent with our previous findings with footshock-induced reinstatement of alcohol seeking in Wistar rats, we found that L822429 attenuates yohimbine-induced reinstatement of alcohol seeking, but does not affect baseline alcohol self-administration. We observed a similar suppression of yohimbine-induced reinstatement of cocaine seeking by L822429, and found that Long-Evans rats exhibit greater sensitivity to NK1R antagonism than Wistar rats. Accordingly, Long-Evans rats exhibit differences in the expression of NK1Rs in some subcortical brain regions. Combined, our findings suggest that while NK1R antagonism differentially influences alcohol- and cocaine-related behavior, this receptor mediates stress-induced seeking of both drugs.</abstract><cop>England</cop><pub>Nature Publishing Group</pub><pmid>24173499</pmid><doi>10.1038/npp.2013.309</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adrenergic alpha-2 Receptor Antagonists - pharmacology Alcohol-Related Disorders - drug therapy Alcohol-Related Disorders - etiology Alcohol-Related Disorders - metabolism Alcoholism Animals Behavior, Addictive - chemically induced Behavior, Addictive - drug therapy Behavior, Addictive - etiology Behavior, Addictive - metabolism Brain Brain - metabolism Central Nervous System Depressants - administration & dosage Central Nervous System Depressants - pharmacology Cocaine Cocaine - administration & dosage Cocaine - pharmacology Cocaine-Related Disorders - drug therapy Cocaine-Related Disorders - etiology Cocaine-Related Disorders - metabolism Dopamine Uptake Inhibitors - administration & dosage Dopamine Uptake Inhibitors - pharmacology Ethanol - administration & dosage Ethanol - pharmacology Extinction Laboratory animals Male Narcotics Neurokinin-1 Receptor Antagonists - pharmacology Original Piperidines - pharmacology Rats Rats, Long-Evans Rats, Wistar Receptors, Neurokinin-1 - metabolism Recurrence Saccharin - administration & dosage Species Specificity Stress, Psychological - chemically induced Stress, Psychological - complications Stress, Psychological - metabolism Yohimbine - pharmacology |
| title | The role of the neurokinin-1 receptor in stress-induced reinstatement of alcohol and cocaine seeking |
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