Cholinergic mu-opioid receptor deletion alters reward preference and aversion-resistance
The endogenous opioid system has been implicated in alcohol consumption and preference in both humans and animals. The mu opioid receptor (MOR) is expressed on multiple cells in the striatum, however little is known about the contributions of specific MOR populations to alcohol drinking behaviors. T...
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description | The endogenous opioid system has been implicated in alcohol consumption and preference in both humans and animals. The mu opioid receptor (MOR) is expressed on multiple cells in the striatum, however little is known about the contributions of specific MOR populations to alcohol drinking behaviors. The current study used mice with a genetic deletion of MOR in cholinergic cells (ChAT-Cre/Oprm1fl/fl) to examine the role of MORs expressed in cholinergic interneurons (CINs) in home cage self-administration paradigms. Male and female ChAT-Cre/Oprm1fl/fl mice were generated and heterozygous Cre+ (knockout) and Cre- (control) mice were tested for alcohol consumption in two drinking paradigms: limited access “Drinking in the Dark” and intermittent access. Quinine was added to the drinking bottles in the DID experiment to test aversion-resistant, “compulsive” drinking. Nicotine and sucrose drinking were also assessed so comparisons could be made with other rewarding substances. Cholinergic MOR deletion did not influence consumption or preference for ethanol (EtOH) in either drinking task. Differences were observed in aversion-resistance in males with Cre + mice tolerating lower concentrations of quinine than Cre-. In contrast to EtOH, preference for nicotine was reduced following cholinergic MOR deletion while sucrose consumption and preference was increased in Cre+ (vs. Cre-) females. Locomotor activity was also greater in females following the deletion. These results suggest that cholinergic MORs participate in preference for rewarding substances. Further, while they are not required for consumption of alcohol alone, cholinergic MORs may influence the tendency to drink despite negative consequences.
•It is not known how specific MOR populations contribute to alcohol drinking.•ChAT-Cre/Oprm1fl/fl mice have MOR deletion on cholinergic neurons.•Cholinergic MOR deletion increased quinine-resistant EtOH consumption in male mice.•Cholinergic MOR deletion decreased preference for nicotine, but not alcohol.•Cholinergic MOR deletion increased sucrose consumption and locomotion in females. |
doi_str_mv | 10.1016/j.neuropharm.2024.110019 |
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•It is not known how specific MOR populations contribute to alcohol drinking.•ChAT-Cre/Oprm1fl/fl mice have MOR deletion on cholinergic neurons.•Cholinergic MOR deletion increased quinine-resistant EtOH consumption in male mice.•Cholinergic MOR deletion decreased preference for nicotine, but not alcohol.•Cholinergic MOR deletion increased sucrose consumption and locomotion in females.</description><identifier>ISSN: 0028-3908</identifier><identifier>ISSN: 1873-7064</identifier><identifier>EISSN: 1873-7064</identifier><identifier>DOI: 10.1016/j.neuropharm.2024.110019</identifier><identifier>PMID: 38810926</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Alcohol ; Alcohol Drinking - genetics ; Alcohol Drinking - psychology ; Animals ; Aversion-resistance ; Avoidance Learning - drug effects ; Avoidance Learning - physiology ; Binge drinking ; Cholinergic neurons ; Cholinergic Neurons - drug effects ; Cholinergic Neurons - metabolism ; Cholinergic Neurons - physiology ; Ethanol - administration & dosage ; Ethanol - pharmacology ; Female ; Interneurons - drug effects ; Interneurons - metabolism ; Interneurons - physiology ; Male ; Mice ; Mice, Knockout ; Mu opioid receptor ; Nicotine ; Nicotine - pharmacology ; Quinine - administration & dosage ; Quinine - pharmacology ; Receptors, Opioid, mu - genetics ; Receptors, Opioid, mu - metabolism ; Reward ; Self Administration ; Sucrose - administration & dosage</subject><ispartof>Neuropharmacology, 2024-09, Vol.255, p.110019, Article 110019</ispartof><rights>2024 Elsevier Ltd</rights><rights>Copyright © 2024 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c249t-4d53fcd133c359637f0b8f0a17538fee80dc7ac9b3ab4115efb45ad0ab51a7883</cites><orcidid>0009-0002-3859-525X ; 0000-0002-8463-7580</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neuropharm.2024.110019$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38810926$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Beane, Cambria R.</creatorcontrib><creatorcontrib>Lewis, Delainey G.</creatorcontrib><creatorcontrib>Bruns VI, Nicolaus</creatorcontrib><creatorcontrib>Pikus, Kat L.</creatorcontrib><creatorcontrib>Durfee, Mary H.</creatorcontrib><creatorcontrib>Zegarelli, Roman A.</creatorcontrib><creatorcontrib>Perry, Thomas W.</creatorcontrib><creatorcontrib>Sandoval, Oscar</creatorcontrib><creatorcontrib>Radke, Anna K.</creatorcontrib><title>Cholinergic mu-opioid receptor deletion alters reward preference and aversion-resistance</title><title>Neuropharmacology</title><addtitle>Neuropharmacology</addtitle><description>The endogenous opioid system has been implicated in alcohol consumption and preference in both humans and animals. The mu opioid receptor (MOR) is expressed on multiple cells in the striatum, however little is known about the contributions of specific MOR populations to alcohol drinking behaviors. The current study used mice with a genetic deletion of MOR in cholinergic cells (ChAT-Cre/Oprm1fl/fl) to examine the role of MORs expressed in cholinergic interneurons (CINs) in home cage self-administration paradigms. Male and female ChAT-Cre/Oprm1fl/fl mice were generated and heterozygous Cre+ (knockout) and Cre- (control) mice were tested for alcohol consumption in two drinking paradigms: limited access “Drinking in the Dark” and intermittent access. Quinine was added to the drinking bottles in the DID experiment to test aversion-resistant, “compulsive” drinking. Nicotine and sucrose drinking were also assessed so comparisons could be made with other rewarding substances. Cholinergic MOR deletion did not influence consumption or preference for ethanol (EtOH) in either drinking task. Differences were observed in aversion-resistance in males with Cre + mice tolerating lower concentrations of quinine than Cre-. In contrast to EtOH, preference for nicotine was reduced following cholinergic MOR deletion while sucrose consumption and preference was increased in Cre+ (vs. Cre-) females. Locomotor activity was also greater in females following the deletion. These results suggest that cholinergic MORs participate in preference for rewarding substances. Further, while they are not required for consumption of alcohol alone, cholinergic MORs may influence the tendency to drink despite negative consequences.
•It is not known how specific MOR populations contribute to alcohol drinking.•ChAT-Cre/Oprm1fl/fl mice have MOR deletion on cholinergic neurons.•Cholinergic MOR deletion increased quinine-resistant EtOH consumption in male mice.•Cholinergic MOR deletion decreased preference for nicotine, but not alcohol.•Cholinergic MOR deletion increased sucrose consumption and locomotion in females.</description><subject>Alcohol</subject><subject>Alcohol Drinking - genetics</subject><subject>Alcohol Drinking - psychology</subject><subject>Animals</subject><subject>Aversion-resistance</subject><subject>Avoidance Learning - drug effects</subject><subject>Avoidance Learning - physiology</subject><subject>Binge drinking</subject><subject>Cholinergic neurons</subject><subject>Cholinergic Neurons - drug effects</subject><subject>Cholinergic Neurons - metabolism</subject><subject>Cholinergic Neurons - physiology</subject><subject>Ethanol - administration & dosage</subject><subject>Ethanol - pharmacology</subject><subject>Female</subject><subject>Interneurons - drug effects</subject><subject>Interneurons - metabolism</subject><subject>Interneurons - physiology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Mu opioid receptor</subject><subject>Nicotine</subject><subject>Nicotine - pharmacology</subject><subject>Quinine - administration & dosage</subject><subject>Quinine - pharmacology</subject><subject>Receptors, Opioid, mu - genetics</subject><subject>Receptors, Opioid, mu - metabolism</subject><subject>Reward</subject><subject>Self Administration</subject><subject>Sucrose - administration & dosage</subject><issn>0028-3908</issn><issn>1873-7064</issn><issn>1873-7064</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1PwzAMhiMEYmPwF1CPXFqcph_pESa-pElcQOIWpYnLMrVNSdoh_j2ZNuDIyZL92Nb7EBJRSCjQ4nqT9Dg5O6yl65IU0iyhFIBWR2ROecniEorsmMwBUh6zCviMnHm_AYCMU35KZoxzClVazMnbcm1b06N7NyrqptgOxhodOVQ4jNZFGlscje0j2Y7ofBh8SqejwWGDDnuFkex1JLdhFqjYoTd-lKF_Tk4a2Xq8ONQFeb2_e1k-xqvnh6flzSpWaVaNcaZz1ihNGVMsrwpWNlDzBiQtc8YbRA5alVJVNZN1RmmOTZ3lUoOscypLztmCXO3vDs5-TOhH0RmvsG1lj3bygkGR5izlVRVQvkeVs96HBGJwppPuS1AQO69iI_68ip1XsfcaVi8PX6a6Q_27-CMyALd7AEPWrUEnvDI7P9oEl6PQ1vz_5RvYQZCo</recordid><startdate>20240901</startdate><enddate>20240901</enddate><creator>Beane, Cambria R.</creator><creator>Lewis, Delainey G.</creator><creator>Bruns VI, Nicolaus</creator><creator>Pikus, Kat L.</creator><creator>Durfee, Mary H.</creator><creator>Zegarelli, Roman A.</creator><creator>Perry, Thomas W.</creator><creator>Sandoval, Oscar</creator><creator>Radke, Anna K.</creator><general>Elsevier Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0009-0002-3859-525X</orcidid><orcidid>https://orcid.org/0000-0002-8463-7580</orcidid></search><sort><creationdate>20240901</creationdate><title>Cholinergic mu-opioid receptor deletion alters reward preference and aversion-resistance</title><author>Beane, Cambria R. ; Lewis, Delainey G. ; Bruns VI, Nicolaus ; Pikus, Kat L. ; Durfee, Mary H. ; Zegarelli, Roman A. ; Perry, Thomas W. ; Sandoval, Oscar ; Radke, Anna K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c249t-4d53fcd133c359637f0b8f0a17538fee80dc7ac9b3ab4115efb45ad0ab51a7883</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Alcohol</topic><topic>Alcohol Drinking - genetics</topic><topic>Alcohol Drinking - psychology</topic><topic>Animals</topic><topic>Aversion-resistance</topic><topic>Avoidance Learning - drug effects</topic><topic>Avoidance Learning - physiology</topic><topic>Binge drinking</topic><topic>Cholinergic neurons</topic><topic>Cholinergic Neurons - drug effects</topic><topic>Cholinergic Neurons - metabolism</topic><topic>Cholinergic Neurons - physiology</topic><topic>Ethanol - administration & dosage</topic><topic>Ethanol - pharmacology</topic><topic>Female</topic><topic>Interneurons - drug effects</topic><topic>Interneurons - metabolism</topic><topic>Interneurons - physiology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Mu opioid receptor</topic><topic>Nicotine</topic><topic>Nicotine - pharmacology</topic><topic>Quinine - administration & dosage</topic><topic>Quinine - pharmacology</topic><topic>Receptors, Opioid, mu - genetics</topic><topic>Receptors, Opioid, mu - metabolism</topic><topic>Reward</topic><topic>Self Administration</topic><topic>Sucrose - administration & dosage</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Beane, Cambria R.</creatorcontrib><creatorcontrib>Lewis, Delainey G.</creatorcontrib><creatorcontrib>Bruns VI, Nicolaus</creatorcontrib><creatorcontrib>Pikus, Kat L.</creatorcontrib><creatorcontrib>Durfee, Mary H.</creatorcontrib><creatorcontrib>Zegarelli, Roman A.</creatorcontrib><creatorcontrib>Perry, Thomas W.</creatorcontrib><creatorcontrib>Sandoval, Oscar</creatorcontrib><creatorcontrib>Radke, Anna K.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neuropharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Beane, Cambria R.</au><au>Lewis, Delainey G.</au><au>Bruns VI, Nicolaus</au><au>Pikus, Kat L.</au><au>Durfee, Mary H.</au><au>Zegarelli, Roman A.</au><au>Perry, Thomas W.</au><au>Sandoval, Oscar</au><au>Radke, Anna K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cholinergic mu-opioid receptor deletion alters reward preference and aversion-resistance</atitle><jtitle>Neuropharmacology</jtitle><addtitle>Neuropharmacology</addtitle><date>2024-09-01</date><risdate>2024</risdate><volume>255</volume><spage>110019</spage><pages>110019-</pages><artnum>110019</artnum><issn>0028-3908</issn><issn>1873-7064</issn><eissn>1873-7064</eissn><abstract>The endogenous opioid system has been implicated in alcohol consumption and preference in both humans and animals. The mu opioid receptor (MOR) is expressed on multiple cells in the striatum, however little is known about the contributions of specific MOR populations to alcohol drinking behaviors. The current study used mice with a genetic deletion of MOR in cholinergic cells (ChAT-Cre/Oprm1fl/fl) to examine the role of MORs expressed in cholinergic interneurons (CINs) in home cage self-administration paradigms. Male and female ChAT-Cre/Oprm1fl/fl mice were generated and heterozygous Cre+ (knockout) and Cre- (control) mice were tested for alcohol consumption in two drinking paradigms: limited access “Drinking in the Dark” and intermittent access. Quinine was added to the drinking bottles in the DID experiment to test aversion-resistant, “compulsive” drinking. Nicotine and sucrose drinking were also assessed so comparisons could be made with other rewarding substances. Cholinergic MOR deletion did not influence consumption or preference for ethanol (EtOH) in either drinking task. Differences were observed in aversion-resistance in males with Cre + mice tolerating lower concentrations of quinine than Cre-. In contrast to EtOH, preference for nicotine was reduced following cholinergic MOR deletion while sucrose consumption and preference was increased in Cre+ (vs. Cre-) females. Locomotor activity was also greater in females following the deletion. These results suggest that cholinergic MORs participate in preference for rewarding substances. Further, while they are not required for consumption of alcohol alone, cholinergic MORs may influence the tendency to drink despite negative consequences.
•It is not known how specific MOR populations contribute to alcohol drinking.•ChAT-Cre/Oprm1fl/fl mice have MOR deletion on cholinergic neurons.•Cholinergic MOR deletion increased quinine-resistant EtOH consumption in male mice.•Cholinergic MOR deletion decreased preference for nicotine, but not alcohol.•Cholinergic MOR deletion increased sucrose consumption and locomotion in females.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>38810926</pmid><doi>10.1016/j.neuropharm.2024.110019</doi><orcidid>https://orcid.org/0009-0002-3859-525X</orcidid><orcidid>https://orcid.org/0000-0002-8463-7580</orcidid></addata></record> |
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subjects | Alcohol Alcohol Drinking - genetics Alcohol Drinking - psychology Animals Aversion-resistance Avoidance Learning - drug effects Avoidance Learning - physiology Binge drinking Cholinergic neurons Cholinergic Neurons - drug effects Cholinergic Neurons - metabolism Cholinergic Neurons - physiology Ethanol - administration & dosage Ethanol - pharmacology Female Interneurons - drug effects Interneurons - metabolism Interneurons - physiology Male Mice Mice, Knockout Mu opioid receptor Nicotine Nicotine - pharmacology Quinine - administration & dosage Quinine - pharmacology Receptors, Opioid, mu - genetics Receptors, Opioid, mu - metabolism Reward Self Administration Sucrose - administration & dosage |
title | Cholinergic mu-opioid receptor deletion alters reward preference and aversion-resistance |
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