{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Martucci LL"],"funding":["Fondation Jérôme Lejeune","Université Paris-Sud","College of Natural Resources and Sciences, Humboldt State University","Institut National de la Santé et de la Recherche Médicale","Centre National de la Recherche Scientifique","Wellcome Trust"],"pagination":["5823-5835"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6677574"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["33(5)"],"pubmed_abstract":["Autism spectrum disorder (ASD) is characterized by early onset of behavioral and cognitive alterations. Low plasma levels of oxytocin (OT) have also been found in ASD patients; recently, a critical role for the enzyme CD38 in the regulation of OT release was demonstrated. CD38 is important in regulating several Ca<sup>2+</sup>-dependent pathways, but beyond its role in regulating OT secretion, it is not known whether a deficit in CD38 expression leads to functional modifications of the prefrontal cortex (PFC), a structure involved in social behavior. Here, we report that CD38<sup>-/-</sup> male mice show an abnormal cortex development, an excitation-inhibition balance shifted toward a higher excitation, and impaired synaptic plasticity in the PFC such as those observed in various mouse mod"],"journal":["FASEB journal : official publication of the Federation of American Societies for Experimental Biology"],"pubmed_title":["A multiscale analysis in CD38<sup>-/-</sup> mice unveils major prefrontal cortex dysfunctions."],"pmcid":["PMC6677574"],"funding_grant_id":["102828/Z/13/Z","102828"],"pubmed_authors":["Launay JM","Fossier P","Vaillend C","Chaussenot R","Sebrie C","de la Porte S","Granon S","Edeline JM","Amar M","Benet G","Bauer O","Cancela JM","Callebert J","de Zelicourt A","Galione A","Nosjean A","Martucci LL"],"additional_accession":[]},"is_claimable":false,"name":"A multiscale analysis in CD38<sup>-/-</sup> mice unveils major prefrontal cortex dysfunctions.","description":"Autism spectrum disorder (ASD) is characterized by early onset of behavioral and cognitive alterations. Low plasma levels of oxytocin (OT) have also been found in ASD patients; recently, a critical role for the enzyme CD38 in the regulation of OT release was demonstrated. CD38 is important in regulating several Ca<sup>2+</sup>-dependent pathways, but beyond its role in regulating OT secretion, it is not known whether a deficit in CD38 expression leads to functional modifications of the prefrontal cortex (PFC), a structure involved in social behavior. Here, we report that CD38<sup>-/-</sup> male mice show an abnormal cortex development, an excitation-inhibition balance shifted toward a higher excitation, and impaired synaptic plasticity in the PFC such as those observed in various mouse mod","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 May","modification":"2026-05-13T16:11:13.236Z","creation":"2019-08-07T07:08:58Z"},"accession":"S-EPMC6677574","cross_references":{"pubmed":["30844310"],"doi":["10.1096/fj.201800489R","10.1096/fj.201800489r"]}}