{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Smedler E"],"funding":["Hj&amp;#x00E4;rnfonden","European Molecular Biology Organization","Vetenskapsr&amp;#x00E5;det","Barncancerfonden","Cancerfonden"],"pagination":["e2108768119"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8851547"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["119(7)"],"pubmed_abstract":["The L-type voltage-gated Ca<sup>2+</sup> channel gene <i>CACNA1C</i> is a risk gene for various psychiatric conditions, including schizophrenia and bipolar disorder. However, the cellular mechanism by which <i>CACNA1C</i> contributes to psychiatric disorders has not been elucidated. Here, we report that the embryonic deletion of <i>Cacna1c</i> in neurons destined for the cerebral cortex using an <i>Emx1-Cre</i> strategy disturbs spontaneous Ca<sup>2+</sup> activity and causes abnormal brain development and anxiety. By combining computational modeling with electrophysiological membrane potential manipulation, we found that neural network activity was driven by intrinsic spontaneous Ca<sup>2+</sup> activity in distinct progenitor cells expressing marginally increased levels of voltage-gated "],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Disrupted <i>Cacna1c</i> gene expression perturbs spontaneous Ca<sup>2+</sup> activity causing abnormal brain development and increased anxiety."],"pmcid":["PMC8851547"],"funding_grant_id":["FO2020-0199","FO2018-0209","CAN 2016-801","2017-00815","19 0545 Us","PR2020-0124","ALTF 596-2014","2021-03108","2013-3189","19 0544 Pj","FO2017-0107","PR2018-0123"],"pubmed_authors":["Brusini I","Masini D","Wang C","Kanatani S","Malmersjo S","Rebellato P","Zhang S","Smedler E","Fisone G","Dehnisch Ellstrom I","West Z","Harkany T","Louhivuori L","Uhlen P","Romanov RA","Caramia M"],"additional_accession":[]},"is_claimable":false,"name":"Disrupted <i>Cacna1c</i> gene expression perturbs spontaneous Ca<sup>2+</sup> activity causing abnormal brain development and increased anxiety.","description":"The L-type voltage-gated Ca<sup>2+</sup> channel gene <i>CACNA1C</i> is a risk gene for various psychiatric conditions, including schizophrenia and bipolar disorder. However, the cellular mechanism by which <i>CACNA1C</i> contributes to psychiatric disorders has not been elucidated. Here, we report that the embryonic deletion of <i>Cacna1c</i> in neurons destined for the cerebral cortex using an <i>Emx1-Cre</i> strategy disturbs spontaneous Ca<sup>2+</sup> activity and causes abnormal brain development and anxiety. By combining computational modeling with electrophysiological membrane potential manipulation, we found that neural network activity was driven by intrinsic spontaneous Ca<sup>2+</sup> activity in distinct progenitor cells expressing marginally increased levels of voltage-gated ","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Feb","modification":"2025-06-01T04:20:18.592Z","creation":"2025-06-01T04:20:18.592Z"},"accession":"S-EPMC8851547","cross_references":{"pubmed":["35135875"],"doi":["10.1073/pnas.2108768119"]}}