{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,10]],"date-time":"2025-10-10T01:57:22Z","timestamp":1760061442513,"version":"3.40.4"},"reference-count":31,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2014,2,25]],"date-time":"2014-02-25T00:00:00Z","timestamp":1393286400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Alcoholism Clin &amp;amp; Exp Res"],"published-print":{"date-parts":[[2014,5]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Initial sensitivity to ethanol (EtOH) and the capacity to develop acute functional tolerance (<jats:styled-content style=\"fixed-case\">AFT<\/jats:styled-content>) to its adverse effects may influence the amount of alcohol consumed and may also predict future alcohol use patterns. The current study assessed sensitivity and<jats:styled-content style=\"fixed-case\">AFT<\/jats:styled-content>to the ataxic and hypnotic effects of EtOH in the first replicate of mice (<jats:styled-content style=\"fixed-case\">HDID<\/jats:styled-content>\u20101) selectively bred for high blood EtOH concentrations (<jats:styled-content style=\"fixed-case\">BEC<\/jats:styled-content>s) following limited access to EtOH in the Drinking in the Dark (<jats:styled-content style=\"fixed-case\">DID<\/jats:styled-content>) paradigm.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Na\u00efve male and female<jats:styled-content style=\"fixed-case\">HDID<\/jats:styled-content>\u20101 and<jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content>\/Npt mice from the progenitor stock were evaluated in 3 separate experiments. In Experiments 1 and 2, EtOH\u2010induced ataxia was assessed using the static dowel task. In Experiment 3, EtOH\u2010induced hypnosis was assessed by using modified restraint tubes to measure the loss of righting reflex (<jats:styled-content style=\"fixed-case\">LORR<\/jats:styled-content>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">HDID<\/jats:styled-content>\u20101 mice exhibited reduced initial sensitivity to both EtOH\u2010induced ataxia (<jats:italic>p\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.001) and hypnosis (<jats:italic>p\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.05) relative to<jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content>\/Npt mice.<jats:styled-content style=\"fixed-case\">AFT<\/jats:styled-content>was calculated by subtracting the<jats:styled-content style=\"fixed-case\">BEC<\/jats:styled-content>at loss of function from the<jats:styled-content style=\"fixed-case\">BEC<\/jats:styled-content>at recovery (Experiments 1 and 3) or by subtracting<jats:styled-content style=\"fixed-case\">BEC<\/jats:styled-content>at an initial recovery from the<jats:styled-content style=\"fixed-case\">BEC<\/jats:styled-content>at a second recovery following an additional alcohol dose (Experiment 2). The dowel test yielded no line differences in<jats:styled-content style=\"fixed-case\">AFT<\/jats:styled-content>, but<jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content>\/Npt mice developed slightly greater<jats:styled-content style=\"fixed-case\">AFT<\/jats:styled-content>to EtOH\u2010induced<jats:styled-content style=\"fixed-case\">LORR<\/jats:styled-content>than<jats:styled-content style=\"fixed-case\">HDID<\/jats:styled-content>\u20101 (<jats:italic>p\u00a0<\/jats:italic>&lt;<jats:italic>\u00a0<\/jats:italic>0.05).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>These results suggest that<jats:styled-content style=\"fixed-case\">HDID<\/jats:styled-content>\u20101 mice exhibit aspects of blunted ataxic and hypnotic sensitivity to EtOH which may influence their high EtOH intake via<jats:styled-content style=\"fixed-case\">DID<\/jats:styled-content>, but do not display widely different development of<jats:styled-content style=\"fixed-case\">AFT<\/jats:styled-content>. These findings differ from previous findings with the high alcohol\u2010preferring (<jats:styled-content style=\"fixed-case\">HAP<\/jats:styled-content>) selected mouse lines, suggesting that genetic predisposition for binge, versus other forms of excessive alcohol consumption, is associated with unique responses to EtOH\u2010induced motor incoordination.<\/jats:p><\/jats:sec>","DOI":"10.1111\/acer.12385","type":"journal-article","created":{"date-parts":[[2014,2,25]],"date-time":"2014-02-25T23:50:58Z","timestamp":1393372258000},"page":"1284-1292","source":"Crossref","is-referenced-by-count":11,"title":["Genetic Relationship Between Predisposition for Binge Alcohol Consumption and Blunted Sensitivity to Adverse Effects of Alcohol in Mice"],"prefix":"10.1111","volume":"38","author":[{"given":"Brandon M.","family":"Fritz","sequence":"first","affiliation":[{"name":"Indiana Alcohol Research Center Department of Psychology Indiana University Purdue University Indianapolis Indianapolis 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