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Intermittent Access to Ethanol Drinking Facilitates the Transition to Excessive Drinking After Chronic Intermittent Ethanol Vapor Exposure
Author(s) -
Kimbrough Adam,
Kim Sarah,
Cole Maury,
Brennan Molly,
George Olivier
Publication year - 2017
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/acer.13434
Subject(s) - ethanol , binge drinking , alcohol , self administration , psychology , alcohol use disorder , medicine , endocrinology , chemistry , alcohol consumption , biochemistry
Background Alcohol binge drinking in humans is thought to increase the risk for alcohol use disorder (AUD). Unclear is whether drinking patterns (e.g., bingelike or stable drinking) differentially affect the transition to compulsive‐like drinking in dependent individuals. We examined whether chronic bingelike drinking facilitates the transition to compulsive‐like drinking in rats. Methods Male Wistar rats were given 5 months of intermittent access to ethanol (EtOH) (IAE) or continuous access to EtOH (CAE) in a 2‐bottle choice paradigm. Then, rats were given chronic intermittent EtOH (CIE) vapor exposure. Escalation of EtOH intake and compulsive‐like responding for EtOH, using a progressive‐ratio schedule of reinforcement and quinine‐adulterated EtOH, were measured. Results IAE rats escalated EtOH drinking after 2 weeks of 2‐bottle choice, whereas CAE rats exhibited stable EtOH drinking for 5 months. After 8 weeks of CIE, both IAE + CIE and CAE + CIE rats escalated their EtOH intake. However, IAE rats escalated their EtOH intake weeks sooner than CAE rats and exhibited greater EtOH intake. No differences in compulsive‐like responding were found between IAE + CIE and CAE + CIE rats. However, both IAE + CIE and CAE + CIE rats showed strong compulsive‐like responding compared with rats without prior IAE or CAE. Conclusions Chronic EtOH drinking at stable or escalated levels for several months is associated with more compulsive‐like responding for EtOH in rats that are exposed to CIE compared with rats without a prior history of EtOH drinking. Moreover, IAE facilitated the transition to compulsive‐like responding for EtOH after CIE exposure, reflected by the escalation of EtOH intake. These results suggest that IAE may facilitate the transition to AUD. This study indicates that despite a moderate level of EtOH drinking, the IAE animal model is highly relevant to early stages of alcohol abuse and suggests that it may be associated with neuroadaptations that produce a faster transition to alcohol dependence.