{"doi":"10.17615/sa9a-w320","title":"Predictors of High Ethanol Consumption in RII?? Knock-Out Mice: Assessment of Anxiety and Ethanol-Induced Sedation","abstract":"Genetic and pharmacological evidence suggests that the cyclic adenosine monophosphate–dependent protein kinase A pathway modulates neurobiological responses to ethanol. Mutant mice lacking the RIIβ subunit of protein kinase A (RIIβ) are resistant to ethanol-induced sedation and drink significantly more ethanol than littermate wild-type mice (RIIβ). We determined whether high ethanol intake by the RIIβ mice on alternate genetic backgrounds is reliably predicted by high basal levels of anxiety or resistance to the sedative effects of ethanol. Two-bottle choice procedures and a battery of behavioral tests (elevated plus maze, open-field activity, and zero maze) were used to assess voluntary ethanol consumption and basal levels of anxiety in RIIβ and RIIβ mice on either a C57BL/6J or a 129/SvEv × C57BL/6J genetic background. Additionally, ethanol-induced sedation and blood ethanol levels were determined in RIIβ and RIIβ mice after intraperitoneal injection of ethanol (3.8 g/kg). RIIβ mice on both genetic backgrounds consumed more ethanol and had a greater preference for ethanol relative to RIIβ mice. However, RIIβ mice showed reduced basal levels of anxiety when maintained on the C57BL/6J background but showed increased anxiety when maintained on the 129/SvEv × C57BL/6J background. Consistent with prior research, RIIβ mice were resistant to the sedative effects of ethanol, regardless of the genetic background. Finally, RIIβ and RIIβ mice showed similar blood ethanol levels. These results indicate that high ethanol consumption is associated with resistance to the sedative effects of ethanol but that basal levels of anxiety, as well as ethanol metabolism, do not reliably predict high ethanol drinking by RIIβ mice.","journal":"UNC Libraries","year":2020,"id":140298,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":0,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9549,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2020-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":600336,"name":"Mitchell J. Picker","orcid":null,"position":1,"is_corresponding":false},{"id":544596,"name":"Jon R. Fee","orcid":null,"position":2,"is_corresponding":false},{"id":384195,"name":"George R. Breese","orcid":null,"position":3,"is_corresponding":false},{"id":497679,"name":"Dennis R. Sparta","orcid":"0000-0003-0060-1693","position":4,"is_corresponding":false},{"id":384192,"name":"Darin J. Knapp","orcid":null,"position":5,"is_corresponding":false},{"id":482675,"name":"Todd E. Thiele","orcid":"0000-0001-8908-9256","position":0,"is_corresponding":true}],"reference_count":0,"raw_metadata":null,"created_at":"2026-07-18T23:17:17.077903Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}