Prior Exposure to THC Increases the Addictive Effects of Nicotine in Rats
Although it is more common for drug abuse to progress from tobacco to cannabis, in many cases cannabis use develops before tobacco use. Epidemiological evidence indicates that prior cannabis use increases the likelihood of becoming dependent on tobacco. To determine whether this effect might be due...
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description | Although it is more common for drug abuse to progress from tobacco to cannabis, in many cases cannabis use develops before tobacco use. Epidemiological evidence indicates that prior cannabis use increases the likelihood of becoming dependent on tobacco. To determine whether this effect might be due to cannabis exposure per se, in addition to any genetic, social, or environmental factors that might contribute, we extended our series of studies on 'gateway drug' effects in animal models of drug abuse. Rats were exposed to THC, the main psychoactive constituent of cannabis, for 3 days (two intraperitoneal injections/day). Then, starting 1 week later, they were allowed to self-administer nicotine intravenously. THC exposure increased the likelihood of acquiring the nicotine self-administration response from 65% in vehicle-exposed rats to 94% in THC-exposed rats. When the price of nicotine was manipulated by increasing the response requirement, THC-exposed rats maintained higher levels of intake than vehicle-exposed rats, indicating that THC exposure increased the value of nicotine reward. These results contrast sharply with our earlier findings that prior THC exposure did not increase the likelihood of rats acquiring either heroin or cocaine self-administration, nor did it increase the reward value of these drugs. The findings obtained here suggest that a history of cannabis exposure might have lasting effects that increase the risk of becoming addicted to nicotine. |
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Epidemiological evidence indicates that prior cannabis use increases the likelihood of becoming dependent on tobacco. To determine whether this effect might be due to cannabis exposure per se, in addition to any genetic, social, or environmental factors that might contribute, we extended our series of studies on 'gateway drug' effects in animal models of drug abuse. Rats were exposed to THC, the main psychoactive constituent of cannabis, for 3 days (two intraperitoneal injections/day). Then, starting 1 week later, they were allowed to self-administer nicotine intravenously. THC exposure increased the likelihood of acquiring the nicotine self-administration response from 65% in vehicle-exposed rats to 94% in THC-exposed rats. When the price of nicotine was manipulated by increasing the response requirement, THC-exposed rats maintained higher levels of intake than vehicle-exposed rats, indicating that THC exposure increased the value of nicotine reward. These results contrast sharply with our earlier findings that prior THC exposure did not increase the likelihood of rats acquiring either heroin or cocaine self-administration, nor did it increase the reward value of these drugs. The findings obtained here suggest that a history of cannabis exposure might have lasting effects that increase the risk of becoming addicted to nicotine.</description><identifier>ISSN: 0893-133X</identifier><identifier>EISSN: 1740-634X</identifier><identifier>DOI: 10.1038/npp.2013.16</identifier><identifier>PMID: 23314220</identifier><identifier>CODEN: NEROEW</identifier><language>eng</language><publisher>Basingstoke: Nature Publishing Group</publisher><subject>Addictions ; Addictive behaviors ; Animals ; Behavior ; Behavior, Addictive - chemically induced ; Behavior, Addictive - psychology ; Biological and medical sciences ; Cannabinoid Receptor Agonists - pharmacology ; Cocaine ; Conditioning, Operant - drug effects ; Dronabinol - pharmacology ; Drug abuse ; Drug dosages ; Drug Synergism ; Epidemiology ; Heroin ; Hypotheses ; Male ; Marijuana ; Medical sciences ; Motor Activity - drug effects ; Nicotine ; Nicotine - administration & dosage ; Nicotine - pharmacology ; Nicotinic Agonists - administration & dosage ; Nicotinic Agonists - pharmacology ; Original ; Pharmacology ; Rats ; Reinforcement Schedule ; Reward ; Self Administration ; Tetrahydrocannabinol ; THC ; Tobacco ; Tobacco, tobacco smoking ; Toxicology</subject><ispartof>Neuropsychopharmacology (New York, N.Y.), 2013-06, Vol.38 (7), p.1198-1208</ispartof><rights>2014 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jun 2013</rights><rights>Copyright © 2013 American College of Neuropsychopharmacology 2013 American College of Neuropsychopharmacology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c472t-3d7deb42edecae5dc70f64fd851922453f1137288c9c5bfba53a3fef267b5deb3</citedby><cites>FETCH-LOGICAL-c472t-3d7deb42edecae5dc70f64fd851922453f1137288c9c5bfba53a3fef267b5deb3</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/PMC3656362/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3656362/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,728,781,785,886,27928,27929,53795,53797</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27374569$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23314220$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>PANLILIO, Leigh V</creatorcontrib><creatorcontrib>ZANETTINI, Claudio</creatorcontrib><creatorcontrib>BARNES, Chanel</creatorcontrib><creatorcontrib>SOLINAS, Marcelo</creatorcontrib><creatorcontrib>GOLDBERG, Steven R</creatorcontrib><title>Prior Exposure to THC Increases the Addictive Effects of Nicotine in Rats</title><title>Neuropsychopharmacology (New York, N.Y.)</title><addtitle>Neuropsychopharmacology</addtitle><description>Although it is more common for drug abuse to progress from tobacco to cannabis, in many cases cannabis use develops before tobacco use. Epidemiological evidence indicates that prior cannabis use increases the likelihood of becoming dependent on tobacco. To determine whether this effect might be due to cannabis exposure per se, in addition to any genetic, social, or environmental factors that might contribute, we extended our series of studies on 'gateway drug' effects in animal models of drug abuse. Rats were exposed to THC, the main psychoactive constituent of cannabis, for 3 days (two intraperitoneal injections/day). Then, starting 1 week later, they were allowed to self-administer nicotine intravenously. THC exposure increased the likelihood of acquiring the nicotine self-administration response from 65% in vehicle-exposed rats to 94% in THC-exposed rats. When the price of nicotine was manipulated by increasing the response requirement, THC-exposed rats maintained higher levels of intake than vehicle-exposed rats, indicating that THC exposure increased the value of nicotine reward. These results contrast sharply with our earlier findings that prior THC exposure did not increase the likelihood of rats acquiring either heroin or cocaine self-administration, nor did it increase the reward value of these drugs. The findings obtained here suggest that a history of cannabis exposure might have lasting effects that increase the risk of becoming addicted to nicotine.</description><subject>Addictions</subject><subject>Addictive behaviors</subject><subject>Animals</subject><subject>Behavior</subject><subject>Behavior, Addictive - chemically induced</subject><subject>Behavior, Addictive - psychology</subject><subject>Biological and medical sciences</subject><subject>Cannabinoid Receptor Agonists - pharmacology</subject><subject>Cocaine</subject><subject>Conditioning, Operant - drug effects</subject><subject>Dronabinol - pharmacology</subject><subject>Drug abuse</subject><subject>Drug dosages</subject><subject>Drug Synergism</subject><subject>Epidemiology</subject><subject>Heroin</subject><subject>Hypotheses</subject><subject>Male</subject><subject>Marijuana</subject><subject>Medical sciences</subject><subject>Motor Activity - drug effects</subject><subject>Nicotine</subject><subject>Nicotine - administration & dosage</subject><subject>Nicotine - 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chemically induced</topic><topic>Behavior, Addictive - psychology</topic><topic>Biological and medical sciences</topic><topic>Cannabinoid Receptor Agonists - pharmacology</topic><topic>Cocaine</topic><topic>Conditioning, Operant - drug effects</topic><topic>Dronabinol - pharmacology</topic><topic>Drug abuse</topic><topic>Drug dosages</topic><topic>Drug Synergism</topic><topic>Epidemiology</topic><topic>Heroin</topic><topic>Hypotheses</topic><topic>Male</topic><topic>Marijuana</topic><topic>Medical sciences</topic><topic>Motor Activity - drug effects</topic><topic>Nicotine</topic><topic>Nicotine - administration & dosage</topic><topic>Nicotine - pharmacology</topic><topic>Nicotinic Agonists - administration & dosage</topic><topic>Nicotinic Agonists - pharmacology</topic><topic>Original</topic><topic>Pharmacology</topic><topic>Rats</topic><topic>Reinforcement Schedule</topic><topic>Reward</topic><topic>Self Administration</topic><topic>Tetrahydrocannabinol</topic><topic>THC</topic><topic>Tobacco</topic><topic>Tobacco, tobacco smoking</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>PANLILIO, Leigh V</creatorcontrib><creatorcontrib>ZANETTINI, Claudio</creatorcontrib><creatorcontrib>BARNES, Chanel</creatorcontrib><creatorcontrib>SOLINAS, Marcelo</creatorcontrib><creatorcontrib>GOLDBERG, Steven R</creatorcontrib><collection>Pascal-Francis</collection><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>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</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>PANLILIO, Leigh V</au><au>ZANETTINI, Claudio</au><au>BARNES, Chanel</au><au>SOLINAS, Marcelo</au><au>GOLDBERG, Steven R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prior Exposure to THC Increases the Addictive Effects of Nicotine in Rats</atitle><jtitle>Neuropsychopharmacology (New York, N.Y.)</jtitle><addtitle>Neuropsychopharmacology</addtitle><date>2013-06-01</date><risdate>2013</risdate><volume>38</volume><issue>7</issue><spage>1198</spage><epage>1208</epage><pages>1198-1208</pages><issn>0893-133X</issn><eissn>1740-634X</eissn><coden>NEROEW</coden><abstract>Although it is more common for drug abuse to progress from tobacco to cannabis, in many cases cannabis use develops before tobacco use. Epidemiological evidence indicates that prior cannabis use increases the likelihood of becoming dependent on tobacco. To determine whether this effect might be due to cannabis exposure per se, in addition to any genetic, social, or environmental factors that might contribute, we extended our series of studies on 'gateway drug' effects in animal models of drug abuse. Rats were exposed to THC, the main psychoactive constituent of cannabis, for 3 days (two intraperitoneal injections/day). Then, starting 1 week later, they were allowed to self-administer nicotine intravenously. THC exposure increased the likelihood of acquiring the nicotine self-administration response from 65% in vehicle-exposed rats to 94% in THC-exposed rats. When the price of nicotine was manipulated by increasing the response requirement, THC-exposed rats maintained higher levels of intake than vehicle-exposed rats, indicating that THC exposure increased the value of nicotine reward. These results contrast sharply with our earlier findings that prior THC exposure did not increase the likelihood of rats acquiring either heroin or cocaine self-administration, nor did it increase the reward value of these drugs. The findings obtained here suggest that a history of cannabis exposure might have lasting effects that increase the risk of becoming addicted to nicotine.</abstract><cop>Basingstoke</cop><pub>Nature Publishing Group</pub><pmid>23314220</pmid><doi>10.1038/npp.2013.16</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Addictions Addictive behaviors Animals Behavior Behavior, Addictive - chemically induced Behavior, Addictive - psychology Biological and medical sciences Cannabinoid Receptor Agonists - pharmacology Cocaine Conditioning, Operant - drug effects Dronabinol - pharmacology Drug abuse Drug dosages Drug Synergism Epidemiology Heroin Hypotheses Male Marijuana Medical sciences Motor Activity - drug effects Nicotine Nicotine - administration & dosage Nicotine - pharmacology Nicotinic Agonists - administration & dosage Nicotinic Agonists - pharmacology Original Pharmacology Rats Reinforcement Schedule Reward Self Administration Tetrahydrocannabinol THC Tobacco Tobacco, tobacco smoking Toxicology |
title | Prior Exposure to THC Increases the Addictive Effects of Nicotine in Rats |
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