<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Bortolato M</submitter><funding>NICHD NIH HHS</funding><funding>NIMH NIH HHS</funding><pagination>2674-88</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3230491</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>36(13)</volume><pubmed_abstract>Monoamine oxidase (MAO)-A is a key enzyme for the degradation of brain serotonin (5-hydroxytryptamine, 5-HT) and norepinephrine (NE). In humans and mice, total MAO-A deficiency results in high 5-HT and NE levels, as well as elevated reactive aggression. Here we report the generation of MAO-A(Neo) mice, a novel line of hypomorphic MAO-A mutants featuring the insertion of a floxed neomycin-resistance cassette in intron-12 of the Maoa gene. This construct resulted in a chimeric, non-functional variant of the Maoa-Neo transcript, with a truncated C-terminus, likely due to aberrant splicing; these deficits notwithstanding, small amounts of functional Maoa transcript were found in the brain of MAO-A(Neo) mice. In the prefrontal cortex and amygdala, MAO-A(Neo) mice showed low, yet detectable, MAO</pubmed_abstract><journal>Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology</journal><pubmed_title>Social deficits and perseverative behaviors, but not overt aggression, in MAO-A hypomorphic mice.</pubmed_title><pmcid>PMC3230491</pmcid><funding_grant_id>R03 MH087794</funding_grant_id><funding_grant_id>R01MH39085</funding_grant_id><funding_grant_id>R37 MH039085</funding_grant_id><funding_grant_id>R03MH087794</funding_grant_id><funding_grant_id>R21 HD070611</funding_grant_id><funding_grant_id>R37MH39085</funding_grant_id><funding_grant_id>R01 MH039085</funding_grant_id><funding_grant_id>R21HD070611</funding_grant_id><pubmed_authors>Scott AL</pubmed_authors><pubmed_authors>Bortolato M</pubmed_authors><pubmed_authors>Shih JC</pubmed_authors><pubmed_authors>Wellman CL</pubmed_authors><pubmed_authors>Chen K</pubmed_authors><pubmed_authors>Godar SC</pubmed_authors><pubmed_authors>Farrell MR</pubmed_authors><pubmed_authors>Chen G</pubmed_authors><pubmed_authors>Rebrin I</pubmed_authors><pubmed_authors>Wu W</pubmed_authors></additional><is_claimable>false</is_claimable><name>Social deficits and perseverative behaviors, but not overt aggression, in MAO-A hypomorphic mice.</name><description>Monoamine oxidase (MAO)-A is a key enzyme for the degradation of brain serotonin (5-hydroxytryptamine, 5-HT) and norepinephrine (NE). In humans and mice, total MAO-A deficiency results in high 5-HT and NE levels, as well as elevated reactive aggression. Here we report the generation of MAO-A(Neo) mice, a novel line of hypomorphic MAO-A mutants featuring the insertion of a floxed neomycin-resistance cassette in intron-12 of the Maoa gene. This construct resulted in a chimeric, non-functional variant of the Maoa-Neo transcript, with a truncated C-terminus, likely due to aberrant splicing; these deficits notwithstanding, small amounts of functional Maoa transcript were found in the brain of MAO-A(Neo) mice. In the prefrontal cortex and amygdala, MAO-A(Neo) mice showed low, yet detectable, MAO</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Dec</publication><modification>2025-07-09T03:04:50.874Z</modification><creation>2025-07-09T03:04:50.874Z</creation></dates><accession>S-EPMC3230491</accession><cross_references><pubmed>21832987</pubmed><doi>10.1038/npp.2011.157</doi></cross_references></HashMap>