{"database":"biostudies-literature","file_versions":[],"scores":{"citationCount":0,"reanalysisCount":0,"viewCount":51,"searchCount":0},"additional":{"submitter":["Clipperton-Allen AE"],"funding":["NIMH NIH HHS","National Institutes of Health"],"pagination":["1366"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8468545"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(9)"],"pubmed_abstract":["<i>Pten</i> germline haploinsufficient (<i>Pten</i><sup>+/-</sup>) mice, which model macrocephaly/autism syndrome, show social and repetitive behavior deficits, early brain overgrowth, and cortical-subcortical hyperconnectivity. Previous work indicated that altered neuronal connectivity may be a substrate for behavioral deficits. We hypothesized that exposing <i>Pten</i><sup>+/-</sup> mice to environmental enrichment after brain overgrowth has occurred may facilitate adaptation to abnormal \"hard-wired\" connectivity through enhancing synaptic plasticity. Thus, we reared <i>Pten</i><sup>+/-</sup> mice and their wild-type littermates from weaning under either standard (4-5 mice per standard-sized cage, containing only bedding and nestlet) or enriched (9-10 mice per large-sized cage, containing objects for exploration and a running wheel, plus bedding and nestlet) conditions. Adult mice were tested on social and non-social assays in which <i>Pten</i><sup>+/-</sup> mice display deficits. Environmental enrichment rescued sex-specific deficits in social behavior in <i>Pten</i><sup>+/-</sup> mice and partially rescued increased repetitive behavior in <i>Pten</i><sup>+/-</sup> males. We found that <i>Pten</i><sup>+/-</sup> mice show increased excitatory and decreased inhibitory pre-synaptic proteins; this phenotype was also rescued by environmental enrichment. Together, our results indicate that environmental enrichment can rescue social behavioral deficits in <i>Pten</i><sup>+/-</sup> mice, possibly through normalizing the excitatory synaptic protein abundance."],"journal":["Genes"],"pubmed_title":["Environmental Enrichment Rescues Social Behavioral Deficits and Synaptic Abnormalities in <i>Pten</i> Haploinsufficient Mice."],"pmcid":["PMC8468545"],"funding_grant_id":["R01 MH108519","R01MH105610, R01MH108519","R01 MH105610"],"pubmed_authors":["Clipperton-Allen AE","Cohen OS","Page DT","Zhang A"],"view_count":["51"],"additional_accession":[]},"is_claimable":false,"name":"Environmental Enrichment Rescues Social Behavioral Deficits and Synaptic Abnormalities in <i>Pten</i> Haploinsufficient Mice.","description":"<i>Pten</i> germline haploinsufficient (<i>Pten</i><sup>+/-</sup>) mice, which model macrocephaly/autism syndrome, show social and repetitive behavior deficits, early brain overgrowth, and cortical-subcortical hyperconnectivity. Previous work indicated that altered neuronal connectivity may be a substrate for behavioral deficits. We hypothesized that exposing <i>Pten</i><sup>+/-</sup> mice to environmental enrichment after brain overgrowth has occurred may facilitate adaptation to abnormal \"hard-wired\" connectivity through enhancing synaptic plasticity. Thus, we reared <i>Pten</i><sup>+/-</sup> mice and their wild-type littermates from weaning under either standard (4-5 mice per standard-sized cage, containing only bedding and nestlet) or enriched (9-10 mice per large-sized cage, containing objects for exploration and a running wheel, plus bedding and nestlet) conditions. Adult mice were tested on social and non-social assays in which <i>Pten</i><sup>+/-</sup> mice display deficits. Environmental enrichment rescued sex-specific deficits in social behavior in <i>Pten</i><sup>+/-</sup> mice and partially rescued increased repetitive behavior in <i>Pten</i><sup>+/-</sup> males. We found that <i>Pten</i><sup>+/-</sup> mice show increased excitatory and decreased inhibitory pre-synaptic proteins; this phenotype was also rescued by environmental enrichment. Together, our results indicate that environmental enrichment can rescue social behavioral deficits in <i>Pten</i><sup>+/-</sup> mice, possibly through normalizing the excitatory synaptic protein abundance.","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Aug","modification":"2024-11-07T02:59:51.366Z","creation":"2022-02-11T11:42:03.521Z"},"accession":"S-EPMC8468545","cross_references":{"pubmed":["34573348"],"doi":["10.3390/genes12091366"]}}