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Selective breeding was carried out to create 2 unique High Drinking in the Dark (HDID\u20101, HDID\u20102) mouse lines that represent models of genetic risk for binge\u2010like drinking. A number of studies have indicated that neuroimmune genes are important for regulation of alcohol drinking. We tested whether compounds shown to reduce drinking in other models also reduce alcohol intake in these unique genetic lines.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We report tests of gabapentin, tesaglitazar, fenofibrate, caffeic acid phenethyl ester (CAPE), ibrutinib, and rolipram. Although these compounds have different mechanisms of action, they have all been shown to reduce inflammatory responses. We evaluated effects of these compounds on alcohol intake. In order to facilitate comparison with previously published findings for some compounds, we employed similar schedules that were previously used for that compound.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Gabapentin increased ethanol (EtOH) binge\u2010like alcohol drinking in female HDID\u20101 and HS\/NPT mice. Tesaglitazar and fenofibrate did not alter 2\u2010bottle choice (2BC) drinking in male HDID\u20101 or HS\/NPT mice. However, tesaglitazar had no effect on DID EtOH intake but reduced blood alcohol levels (BAL), and fenofibrate increased DID intake with no effects on BAL. CAPE had no effect on EtOH intake. Ibrutinib reduced intake in female HDID\u20101 in initial testing, but did not reduce intake in a second week of testing. Rolipram reduced DID intake and BALs in male and female HDID\u20101, HDID\u20102, and HS\/NPT mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>A number of compounds shown to reduce EtOH drinking in other models, and genotypes are not effective in HDID mice or their genetically heterogeneous founders, HS\/NPT. The most promising compound was the PDE4 inhibitor, rolipram. These results highlight the importance of assessing generalizability when rigorously testing compounds for therapeutic development.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/acer.14269","type":"journal-article","created":{"date-parts":[[2019,12,19]],"date-time":"2019-12-19T02:36:27Z","timestamp":1576722987000},"page":"553-566","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":30,"title":["Effects of Pharmacologically Targeting Neuroimmune Pathways on Alcohol Drinking in Mice Selectively Bred to Drink to Intoxication"],"prefix":"10.1111","volume":"44","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8387-1156","authenticated-orcid":false,"given":"Angela R.","family":"Ozburn","sequence":"first","affiliation":[{"name":"Department of Behavioral Neuroscience Portland Alcohol Research Center VA Portland Health Care System Oregon Health &amp; Science University Portland 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