<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lauffer M</submitter><funding>National Center for Advancing Translational Sciences</funding><funding>NCATS NIH HHS</funding><funding>NIMH NIH HHS</funding><funding>National Institute of Mental Health</funding><funding>Roy J. Carver Charitable Trust</funding><pagination>e12791</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9744532</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>21(2)</volume><pubmed_abstract>L-type voltage-gated calcium channels are important regulators of neuronal activity and are widely expressed throughout the brain. One of the major L-type voltage-gated calcium channel isoforms in the brain is Ca&lt;sub>V&lt;/sub> 1.3. Mice lacking Ca&lt;sub>V&lt;/sub> 1.3 are reported to have impairments in fear conditioning and depressive-like behaviors, which have been linked to Ca&lt;sub>V&lt;/sub> 1.3 function in the hippocampus and amygdala. Genetic variation in Ca&lt;sub>V&lt;/sub> 1.3 has been linked to a variety of psychiatric disorders, including autism and schizophrenia, which are associated with altered motor learning, associative learning and social function. Here, we explored whether Ca&lt;sub>V&lt;/sub> 1.3 plays a role in these behaviors. We found that Ca&lt;sub>V&lt;/sub> 1.3 knockout mice have deficits in r</pubmed_abstract><journal>Genes, brain, and behavior</journal><pubmed_title>Deletion of the voltage-gated calcium channel, Ca&lt;sub>V&lt;/sub> 1.3, causes deficits in motor performance and associative learning.</pubmed_title><pmcid>PMC9744532</pmcid><funding_grant_id>R01MH118240</funding_grant_id><funding_grant_id>KL2TR002536</funding_grant_id><funding_grant_id>R01 MH118240</funding_grant_id><funding_grant_id>K01MH106824</funding_grant_id><funding_grant_id>KL2 TR002536</funding_grant_id><pubmed_authors>Wen H</pubmed_authors><pubmed_authors>Myers B</pubmed_authors><pubmed_authors>Parker K</pubmed_authors><pubmed_authors>Williams A</pubmed_authors><pubmed_authors>Lauffer M</pubmed_authors><pubmed_authors>Plumb A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Deletion of the voltage-gated calcium channel, Ca&lt;sub>V&lt;/sub> 1.3, causes deficits in motor performance and associative learning.</name><description>L-type voltage-gated calcium channels are important regulators of neuronal activity and are widely expressed throughout the brain. One of the major L-type voltage-gated calcium channel isoforms in the brain is Ca&lt;sub>V&lt;/sub> 1.3. Mice lacking Ca&lt;sub>V&lt;/sub> 1.3 are reported to have impairments in fear conditioning and depressive-like behaviors, which have been linked to Ca&lt;sub>V&lt;/sub> 1.3 function in the hippocampus and amygdala. Genetic variation in Ca&lt;sub>V&lt;/sub> 1.3 has been linked to a variety of psychiatric disorders, including autism and schizophrenia, which are associated with altered motor learning, associative learning and social function. Here, we explored whether Ca&lt;sub>V&lt;/sub> 1.3 plays a role in these behaviors. We found that Ca&lt;sub>V&lt;/sub> 1.3 knockout mice have deficits in r</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Feb</publication><modification>2025-04-18T23:26:47.331Z</modification><creation>2025-04-07T11:00:30.177Z</creation></dates><accession>S-EPMC9744532</accession><cross_references><pubmed>35044095</pubmed><doi>10.1111/gbb.12791</doi></cross_references></HashMap>