{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Petit EI"],"funding":["Medical Research Council"],"pagination":["1349-1360"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5437891"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["42(6)"],"pubmed_abstract":["Dysbindin-1, a protein that regulates aspects of early and late brain development, has been implicated in the pathobiology of schizophrenia. As the functional roles of the three major isoforms of dysbindin-1, (A, B, and C) remain unknown, we generated a novel mutant mouse, dys-1A<sup>-/-</sup>, with selective loss of dysbindin-1A and investigated schizophrenia-related phenotypes in both males and females. Loss of dysbindin-1A resulted in heightened initial exploration and disruption in subsequent habituation to a novel environment, together with heightened anxiety-related behavior in a stressful environment. Loss of dysbindin-1A was not associated with disruption of either long-term (olfactory) memory or spontaneous alternation behavior. However, dys-1A<sup>-/-</sup> showed enhancement in delay-dependent working memory under high levels of interference relative to controls, ie, impairment in sensitivity to the disruptive effect of such interference. These findings in dys-1A<sup>-/-</sup> provide the first evidence for differential functional roles for dysbindin-1A vs dysbindin-1C isoforms among phenotypes relevant to the pathobiology of schizophrenia. Future studies should investigate putative sex differences in these phenotypic effects."],"journal":["Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology"],"pubmed_title":["Dysregulation of Specialized Delay/Interference-Dependent Working Memory Following Loss of Dysbindin-1A in Schizophrenia-Related Phenotypes."],"pmcid":["PMC5437891"],"funding_grant_id":["MR/L010305/1"],"pubmed_authors":["Morrison AD","Wilson S","Joel J","Shaw A","Kew JN","Henshall DC","Kirby BP","O'Tuathaigh CM","Shapland EM","Tighe O","Clarke N","Sheardown SA","Talbot K","Waddington JL","Petit EI","Michalak Z","Cox R","Blake D"],"additional_accession":[]},"is_claimable":false,"name":"Dysregulation of Specialized Delay/Interference-Dependent Working Memory Following Loss of Dysbindin-1A in Schizophrenia-Related Phenotypes.","description":"Dysbindin-1, a protein that regulates aspects of early and late brain development, has been implicated in the pathobiology of schizophrenia. As the functional roles of the three major isoforms of dysbindin-1, (A, B, and C) remain unknown, we generated a novel mutant mouse, dys-1A<sup>-/-</sup>, with selective loss of dysbindin-1A and investigated schizophrenia-related phenotypes in both males and females. Loss of dysbindin-1A resulted in heightened initial exploration and disruption in subsequent habituation to a novel environment, together with heightened anxiety-related behavior in a stressful environment. Loss of dysbindin-1A was not associated with disruption of either long-term (olfactory) memory or spontaneous alternation behavior. However, dys-1A<sup>-/-</sup> showed enhancement in delay-dependent working memory under high levels of interference relative to controls, ie, impairment in sensitivity to the disruptive effect of such interference. These findings in dys-1A<sup>-/-</sup> provide the first evidence for differential functional roles for dysbindin-1A vs dysbindin-1C isoforms among phenotypes relevant to the pathobiology of schizophrenia. Future studies should investigate putative sex differences in these phenotypic effects.","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 May","modification":"2025-04-19T19:02:55.34Z","creation":"2019-03-26T23:34:01Z"},"accession":"S-EPMC5437891","cross_references":{"pubmed":["27986973"],"doi":["10.1038/npp.2016.282"]}}