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http://purl.uniprot.org/citations/22189290http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22189290http://www.w3.org/2000/01/rdf-schema#comment"The X-linked gene STS encodes the steroid hormone-modulating enzyme steroid sulfatase. Loss-of-function of STS, and variation within the gene, have been associated with vulnerability to developing attention deficit hyperactivity disorder (ADHD), a neurodevelopmental condition characterized by inattention, severe impulsivity, hyperactivity, and motivational deficits. ADHD is commonly comorbid with a variety of disorders, including obsessive-compulsive disorder. The neurobiological role of steroid sulfatase, and therefore its potential role in ADHD and associated comorbidities, is currently poorly understood. The 39,X(Y)*O mouse, which lacks the Sts gene, exhibits several behavioral abnormalities relevant to ADHD including inattention and hyperactivity. Here, we show that, unexpectedly, 39,X(Y)*O mice achieve higher ratios than wild-type mice on a progressive ratio (PR) task thought to index motivation, but that there is no difference between the two groups on a behavioral task thought to index compulsivity (marble burying). High performance liquid chromatography analysis of monoamine levels in wild type and 39,X(Y)*O brain tissue regions (the frontal cortex, striatum, thalamus, hippocampus, and cerebellum) revealed significantly higher levels of 5-hydroxytryptamine (5-HT) in the striatum and hippocampus of 39,X(Y)*O mice. Significant correlations between hippocampal 5-HT levels and PR performance, and between striatal 5-HT levels and locomotor activity strongly implicate regionally-specific perturbations of the 5-HT system as a neurobiological candidate for behavioral differences between 40,XY and 39,X(Y)*O mice. These data suggest that inactivating mutations and functional variants within STS might exert their influence on ADHD vulnerability, and disorder endophenotypes through modulation of the serotonergic system."xsd:string
http://purl.uniprot.org/citations/22189290http://purl.org/dc/terms/identifier"doi:10.1038/npp.2011.314"xsd:string
http://purl.uniprot.org/citations/22189290http://purl.uniprot.org/core/author"Davies W."xsd:string
http://purl.uniprot.org/citations/22189290http://purl.uniprot.org/core/author"Ojarikre O.A."xsd:string
http://purl.uniprot.org/citations/22189290http://purl.uniprot.org/core/author"Humby T."xsd:string
http://purl.uniprot.org/citations/22189290http://purl.uniprot.org/core/author"Cassano T."xsd:string
http://purl.uniprot.org/citations/22189290http://purl.uniprot.org/core/author"Trent S."xsd:string
http://purl.uniprot.org/citations/22189290http://purl.uniprot.org/core/author"Bedse G."xsd:string
http://purl.uniprot.org/citations/22189290http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22189290http://purl.uniprot.org/core/name"Neuropsychopharmacology"xsd:string
http://purl.uniprot.org/citations/22189290http://purl.uniprot.org/core/pages"1267-1274"xsd:string
http://purl.uniprot.org/citations/22189290http://purl.uniprot.org/core/title"Altered serotonergic function may partially account for behavioral endophenotypes in steroid sulfatase-deficient mice."xsd:string
http://purl.uniprot.org/citations/22189290http://purl.uniprot.org/core/volume"37"xsd:string
http://purl.uniprot.org/citations/22189290http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/22189290
http://purl.uniprot.org/citations/22189290http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/22189290
http://purl.uniprot.org/uniprot/#_P50427-mappedCitation-22189290http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22189290
http://purl.uniprot.org/uniprot/P50427http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/22189290