<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Martucci LL</submitter><funding>Fondation Jérôme Lejeune</funding><funding>Université Paris-Sud</funding><funding>College of Natural Resources and Sciences, Humboldt State University</funding><funding>Institut National de la Santé et de la Recherche Médicale</funding><funding>Centre National de la Recherche Scientifique</funding><funding>Wellcome Trust</funding><pagination>5823-5835</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6677574</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>33(5)</volume><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&lt;sup>2+&lt;/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&lt;sup>-/-&lt;/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</pubmed_abstract><journal>FASEB journal : official publication of the Federation of American Societies for Experimental Biology</journal><pubmed_title>A multiscale analysis in CD38&lt;sup>-/-&lt;/sup> mice unveils major prefrontal cortex dysfunctions.</pubmed_title><pmcid>PMC6677574</pmcid><funding_grant_id>102828/Z/13/Z</funding_grant_id><funding_grant_id>102828</funding_grant_id><pubmed_authors>Launay JM</pubmed_authors><pubmed_authors>Fossier P</pubmed_authors><pubmed_authors>Vaillend C</pubmed_authors><pubmed_authors>Chaussenot R</pubmed_authors><pubmed_authors>Sebrie C</pubmed_authors><pubmed_authors>de la Porte S</pubmed_authors><pubmed_authors>Granon S</pubmed_authors><pubmed_authors>Edeline JM</pubmed_authors><pubmed_authors>Amar M</pubmed_authors><pubmed_authors>Benet G</pubmed_authors><pubmed_authors>Bauer O</pubmed_authors><pubmed_authors>Cancela JM</pubmed_authors><pubmed_authors>Callebert J</pubmed_authors><pubmed_authors>de Zelicourt A</pubmed_authors><pubmed_authors>Galione A</pubmed_authors><pubmed_authors>Nosjean A</pubmed_authors><pubmed_authors>Martucci LL</pubmed_authors></additional><is_claimable>false</is_claimable><name>A multiscale analysis in CD38&lt;sup>-/-&lt;/sup> mice unveils major prefrontal cortex dysfunctions.</name><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&lt;sup>2+&lt;/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&lt;sup>-/-&lt;/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</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 May</publication><modification>2026-05-13T16:11:13.236Z</modification><creation>2019-08-07T07:08:58Z</creation></dates><accession>S-EPMC6677574</accession><cross_references><pubmed>30844310</pubmed><doi>10.1096/fj.201800489R</doi><doi>10.1096/fj.201800489r</doi></cross_references></HashMap>