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Chronic Intermittent Ethanol Exposure Increases Ethanol Consumption Following Traumatic Stress Exposure in Mice
Individuals with post-traumatic stress disorder (PTSD) often use alcohol to cope with their distress. This aberrant use of alcohol often develops into alcohol use disorder (AUD) leading to high rates of PTSD-AUD co-occurrence. Individuals with comorbid PTSD-AUD have more intense alcohol cravings and...
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Published in: | Frontiers in behavioral neuroscience 2020-06, Vol.14, p.114-114 |
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description | Individuals with post-traumatic stress disorder (PTSD) often use alcohol to cope with their distress. This aberrant use of alcohol often develops into alcohol use disorder (AUD) leading to high rates of PTSD-AUD co-occurrence. Individuals with comorbid PTSD-AUD have more intense alcohol cravings and increased relapse rates during withdrawal than those with AUD alone. In addition, individuals with PTSD or AUD alone often show similar psychological behaviors, such as impulsivity and anhedonia. Extensive clinical studies on the behavioral effects of PTSD-AUD comorbidity, namely alcohol use, have been performed. However, these effects have not been well studied or mechanistically explored in animal models. Therefore, the present study evaluated the effects of traumatic stress comorbid with alcohol exposures on ethanol intake, impulsivity, and anhedonia in mice. Adult male C57Bl/6 mice were first exposed to either mouse single-prolonged stress (mSPS), an animal model that has been validated for characteristics akin to PTSD symptoms, or control conditions. Baseline two-bottle choice ethanol consumption and preference tests were conducted after a 7-day isolation period, as part of the mSPS exposure. Next, mice were exposed to air or chronic intermittent ethanol (CIE), a vapor-induced ethanol dependence and withdrawal model, for 4 weeks. Two-bottle choice ethanol drinking was used to measure dependence-induced ethanol consumption and preference during periods intervening CIE cycles. The novelty suppressed feeding (NSF) test was used to evaluate impulsivity and anhedonia behaviors 48 h after mSPS and/or repeated CIE exposure. Results showed that, compared to control conditions, mSPS did not affect baseline ethanol consumption and preference. However, mSPS-CIE mice increased Post-CIE ethanol consumption compared to Control-Air mice. Mice exposed to mSPS had a shorter latency to feed during the NSF, whereas CIE-exposed mice consumed less palatable food reward in their home cage after the NSF. These results demonstrate that mice exposed to both mSPS and CIE are more vulnerable to ethanol withdrawal effects, and those exposed to mSPS have increased impulsivity, while CIE exposure increases anhedonia. Future studies to examine the relationship between behavioral outcomes and the molecular mechanisms in the brain after PTSD-AUD are warranted. |
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This aberrant use of alcohol often develops into alcohol use disorder (AUD) leading to high rates of PTSD-AUD co-occurrence. Individuals with comorbid PTSD-AUD have more intense alcohol cravings and increased relapse rates during withdrawal than those with AUD alone. In addition, individuals with PTSD or AUD alone often show similar psychological behaviors, such as impulsivity and anhedonia. Extensive clinical studies on the behavioral effects of PTSD-AUD comorbidity, namely alcohol use, have been performed. However, these effects have not been well studied or mechanistically explored in animal models. Therefore, the present study evaluated the effects of traumatic stress comorbid with alcohol exposures on ethanol intake, impulsivity, and anhedonia in mice. Adult male C57Bl/6 mice were first exposed to either mouse single-prolonged stress (mSPS), an animal model that has been validated for characteristics akin to PTSD symptoms, or control conditions. Baseline two-bottle choice ethanol consumption and preference tests were conducted after a 7-day isolation period, as part of the mSPS exposure. Next, mice were exposed to air or chronic intermittent ethanol (CIE), a vapor-induced ethanol dependence and withdrawal model, for 4 weeks. Two-bottle choice ethanol drinking was used to measure dependence-induced ethanol consumption and preference during periods intervening CIE cycles. The novelty suppressed feeding (NSF) test was used to evaluate impulsivity and anhedonia behaviors 48 h after mSPS and/or repeated CIE exposure. Results showed that, compared to control conditions, mSPS did not affect baseline ethanol consumption and preference. However, mSPS-CIE mice increased Post-CIE ethanol consumption compared to Control-Air mice. Mice exposed to mSPS had a shorter latency to feed during the NSF, whereas CIE-exposed mice consumed less palatable food reward in their home cage after the NSF. These results demonstrate that mice exposed to both mSPS and CIE are more vulnerable to ethanol withdrawal effects, and those exposed to mSPS have increased impulsivity, while CIE exposure increases anhedonia. Future studies to examine the relationship between behavioral outcomes and the molecular mechanisms in the brain after PTSD-AUD are warranted.</description><identifier>ISSN: 1662-5153</identifier><identifier>EISSN: 1662-5153</identifier><identifier>DOI: 10.3389/fnbeh.2020.00114</identifier><identifier>PMID: 32694985</identifier><language>eng</language><publisher>Lausanne: Frontiers Research Foundation</publisher><subject>Alcohol ; Alcohol use ; alcohol use disorder ; Animal models ; Behavior ; Behavioral Neuroscience ; chronic intermittent ethanol ; Comorbidity ; Drinking behavior ; Drinking water ; Drug dependence ; Ethanol ; ethanol consumption ; Food ; Hedonic response ; Impulsive behavior ; Impulsivity ; Laboratory animals ; Latency ; Molecular modelling ; mouse single-prolonged stress ; Post traumatic stress disorder ; Preferences ; Reinforcement ; Withdrawal</subject><ispartof>Frontiers in behavioral neuroscience, 2020-06, Vol.14, p.114-114</ispartof><rights>2020. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Copyright © 2020 Piggott, Lloyd, Perrine and Conti. 2020 Piggott, Lloyd, Perrine and Conti</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c467t-f782ee7896711a7c4bcbe5850bf974ed699e07b6ad3614622eb4738babe8d6813</citedby><cites>FETCH-LOGICAL-c467t-f782ee7896711a7c4bcbe5850bf974ed699e07b6ad3614622eb4738babe8d6813</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2418884580/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2418884580?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,882,25734,27905,27906,36993,36994,44571,53772,53774,74875</link.rule.ids></links><search><creatorcontrib>Piggott, Veronica M.</creatorcontrib><creatorcontrib>Lloyd, Scott C.</creatorcontrib><creatorcontrib>Perrine, Shane A.</creatorcontrib><creatorcontrib>Conti, Alana C.</creatorcontrib><title>Chronic Intermittent Ethanol Exposure Increases Ethanol Consumption Following Traumatic Stress Exposure in Mice</title><title>Frontiers in behavioral neuroscience</title><description>Individuals with post-traumatic stress disorder (PTSD) often use alcohol to cope with their distress. This aberrant use of alcohol often develops into alcohol use disorder (AUD) leading to high rates of PTSD-AUD co-occurrence. Individuals with comorbid PTSD-AUD have more intense alcohol cravings and increased relapse rates during withdrawal than those with AUD alone. In addition, individuals with PTSD or AUD alone often show similar psychological behaviors, such as impulsivity and anhedonia. Extensive clinical studies on the behavioral effects of PTSD-AUD comorbidity, namely alcohol use, have been performed. However, these effects have not been well studied or mechanistically explored in animal models. Therefore, the present study evaluated the effects of traumatic stress comorbid with alcohol exposures on ethanol intake, impulsivity, and anhedonia in mice. Adult male C57Bl/6 mice were first exposed to either mouse single-prolonged stress (mSPS), an animal model that has been validated for characteristics akin to PTSD symptoms, or control conditions. Baseline two-bottle choice ethanol consumption and preference tests were conducted after a 7-day isolation period, as part of the mSPS exposure. Next, mice were exposed to air or chronic intermittent ethanol (CIE), a vapor-induced ethanol dependence and withdrawal model, for 4 weeks. Two-bottle choice ethanol drinking was used to measure dependence-induced ethanol consumption and preference during periods intervening CIE cycles. The novelty suppressed feeding (NSF) test was used to evaluate impulsivity and anhedonia behaviors 48 h after mSPS and/or repeated CIE exposure. Results showed that, compared to control conditions, mSPS did not affect baseline ethanol consumption and preference. However, mSPS-CIE mice increased Post-CIE ethanol consumption compared to Control-Air mice. Mice exposed to mSPS had a shorter latency to feed during the NSF, whereas CIE-exposed mice consumed less palatable food reward in their home cage after the NSF. These results demonstrate that mice exposed to both mSPS and CIE are more vulnerable to ethanol withdrawal effects, and those exposed to mSPS have increased impulsivity, while CIE exposure increases anhedonia. Future studies to examine the relationship between behavioral outcomes and the molecular mechanisms in the brain after PTSD-AUD are warranted.</description><subject>Alcohol</subject><subject>Alcohol use</subject><subject>alcohol use disorder</subject><subject>Animal models</subject><subject>Behavior</subject><subject>Behavioral Neuroscience</subject><subject>chronic intermittent ethanol</subject><subject>Comorbidity</subject><subject>Drinking behavior</subject><subject>Drinking water</subject><subject>Drug dependence</subject><subject>Ethanol</subject><subject>ethanol consumption</subject><subject>Food</subject><subject>Hedonic response</subject><subject>Impulsive behavior</subject><subject>Impulsivity</subject><subject>Laboratory animals</subject><subject>Latency</subject><subject>Molecular modelling</subject><subject>mouse single-prolonged stress</subject><subject>Post traumatic stress disorder</subject><subject>Preferences</subject><subject>Reinforcement</subject><subject>Withdrawal</subject><issn>1662-5153</issn><issn>1662-5153</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpdkkuPEzEQhEcIxC6BO8eRuHBJ8Gv8uCChKAuRFnFgOVu2pydxNGMH28Pj3-Mkq4Xl1FZX6VOpXU3zGqMVpVK9G4KF_YogglYIYcyeNNeYc7LscEef_vO-al7kfECIE87E8-aKEq6Ykt11E9f7FIN37TYUSJMvBUJpN2VvQhzbza9jzHOCqroEJkN-kNYx5Hk6Fh9DexPHMf70YdfeJTNPplTe15Ig578EH9rP3sHL5tlgxgyv7uei-XazuVt_Wt5--bhdf7hdOsZFWQ5CEgAhFRcYG-GYdRY62SE7KMGg50oBEpabnnLMOCFgmaDSGguy5xLTRbO9cPtoDvqY_GTSbx2N1-dFTDttUs05glZMEmModJwSJlxvhUTG9lgphVlvTWW9v7COs52gd_VCyYyPoI-V4Pd6F39oUT-JV-yieXsPSPH7DLnoyWcH42gCxDlrwgjHkqLulPvNf9ZDnFOop6ouLKVknUTVhS4ul2LOCYaHMBjpUzP0uRn61Ax9bgb9AwhirXA</recordid><startdate>20200630</startdate><enddate>20200630</enddate><creator>Piggott, Veronica M.</creator><creator>Lloyd, Scott C.</creator><creator>Perrine, Shane A.</creator><creator>Conti, Alana C.</creator><general>Frontiers Research Foundation</general><general>Frontiers Media S.A</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7XB</scope><scope>88I</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20200630</creationdate><title>Chronic Intermittent Ethanol Exposure Increases Ethanol Consumption Following Traumatic Stress Exposure in Mice</title><author>Piggott, Veronica M. ; 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This aberrant use of alcohol often develops into alcohol use disorder (AUD) leading to high rates of PTSD-AUD co-occurrence. Individuals with comorbid PTSD-AUD have more intense alcohol cravings and increased relapse rates during withdrawal than those with AUD alone. In addition, individuals with PTSD or AUD alone often show similar psychological behaviors, such as impulsivity and anhedonia. Extensive clinical studies on the behavioral effects of PTSD-AUD comorbidity, namely alcohol use, have been performed. However, these effects have not been well studied or mechanistically explored in animal models. Therefore, the present study evaluated the effects of traumatic stress comorbid with alcohol exposures on ethanol intake, impulsivity, and anhedonia in mice. Adult male C57Bl/6 mice were first exposed to either mouse single-prolonged stress (mSPS), an animal model that has been validated for characteristics akin to PTSD symptoms, or control conditions. Baseline two-bottle choice ethanol consumption and preference tests were conducted after a 7-day isolation period, as part of the mSPS exposure. Next, mice were exposed to air or chronic intermittent ethanol (CIE), a vapor-induced ethanol dependence and withdrawal model, for 4 weeks. Two-bottle choice ethanol drinking was used to measure dependence-induced ethanol consumption and preference during periods intervening CIE cycles. The novelty suppressed feeding (NSF) test was used to evaluate impulsivity and anhedonia behaviors 48 h after mSPS and/or repeated CIE exposure. Results showed that, compared to control conditions, mSPS did not affect baseline ethanol consumption and preference. However, mSPS-CIE mice increased Post-CIE ethanol consumption compared to Control-Air mice. Mice exposed to mSPS had a shorter latency to feed during the NSF, whereas CIE-exposed mice consumed less palatable food reward in their home cage after the NSF. These results demonstrate that mice exposed to both mSPS and CIE are more vulnerable to ethanol withdrawal effects, and those exposed to mSPS have increased impulsivity, while CIE exposure increases anhedonia. Future studies to examine the relationship between behavioral outcomes and the molecular mechanisms in the brain after PTSD-AUD are warranted.</abstract><cop>Lausanne</cop><pub>Frontiers Research Foundation</pub><pmid>32694985</pmid><doi>10.3389/fnbeh.2020.00114</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Alcohol Alcohol use alcohol use disorder Animal models Behavior Behavioral Neuroscience chronic intermittent ethanol Comorbidity Drinking behavior Drinking water Drug dependence Ethanol ethanol consumption Food Hedonic response Impulsive behavior Impulsivity Laboratory animals Latency Molecular modelling mouse single-prolonged stress Post traumatic stress disorder Preferences Reinforcement Withdrawal |
title | Chronic Intermittent Ethanol Exposure Increases Ethanol Consumption Following Traumatic Stress Exposure in Mice |
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