Pravda Quiñones-Labernik, Kelsey L Blocklinger, Matthew R Bruce, Emily Hagan, Danielle Preuschl, Charlotte Tesar, Sarah L Ferri
{"title":"在野生型小鼠中,过多的新生儿睾酮会导致雄性特有的社交和恐惧记忆缺陷。","authors":"Pravda Quiñones-Labernik, Kelsey L Blocklinger, Matthew R Bruce, Emily Hagan, Danielle Preuschl, Charlotte Tesar, Sarah L Ferri","doi":"10.1523/ENEURO.0020-25.2025","DOIUrl":null,"url":null,"abstract":"<p><p>Neurodevelopmental disorders disproportionately affect males compared with females. The biological mechanisms of this male susceptibility or female protection have not been identified. There is evidence that fetal/neonatal gonadal hormones, which play a pivotal role in many aspects of development, may contribute. Here, we investigate the effects of excess testosterone (T) during a critical period of sex-specific brain organization on social approach and fear learning behaviors in C57BL/6J wild-type mice. Male, but not female, mice treated with T on the day of birth (Postnatal Day 0; PN0) exhibited decreased social approach as juveniles and decreased contextual fear memory as adults, compared with vehicle (veh)-treated controls. These deficits were not driven by anxiety-like behavior or changes in locomotion or body weight. Mice treated with the same dose of T on PN18, which is outside of the critical period of brain masculinization, did not demonstrate impairments compared with the veh group. These findings indicate that excess T during a critical period of early development, but not shortly after, induces long-term deficits relevant to the male sex bias in neurodevelopmental disorders.</p>","PeriodicalId":11617,"journal":{"name":"eNeuro","volume":" ","pages":""},"PeriodicalIF":2.7000,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320760/pdf/","citationCount":"0","resultStr":"{\"title\":\"Excess Neonatal Testosterone Causes Male-Specific Social and Fear Memory Deficits in Wild-Type Mice.\",\"authors\":\"Pravda Quiñones-Labernik, Kelsey L Blocklinger, Matthew R Bruce, Emily Hagan, Danielle Preuschl, Charlotte Tesar, Sarah L Ferri\",\"doi\":\"10.1523/ENEURO.0020-25.2025\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Neurodevelopmental disorders disproportionately affect males compared with females. The biological mechanisms of this male susceptibility or female protection have not been identified. There is evidence that fetal/neonatal gonadal hormones, which play a pivotal role in many aspects of development, may contribute. Here, we investigate the effects of excess testosterone (T) during a critical period of sex-specific brain organization on social approach and fear learning behaviors in C57BL/6J wild-type mice. Male, but not female, mice treated with T on the day of birth (Postnatal Day 0; PN0) exhibited decreased social approach as juveniles and decreased contextual fear memory as adults, compared with vehicle (veh)-treated controls. These deficits were not driven by anxiety-like behavior or changes in locomotion or body weight. Mice treated with the same dose of T on PN18, which is outside of the critical period of brain masculinization, did not demonstrate impairments compared with the veh group. These findings indicate that excess T during a critical period of early development, but not shortly after, induces long-term deficits relevant to the male sex bias in neurodevelopmental disorders.</p>\",\"PeriodicalId\":11617,\"journal\":{\"name\":\"eNeuro\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":2.7000,\"publicationDate\":\"2025-08-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12320760/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"eNeuro\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1523/ENEURO.0020-25.2025\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"eNeuro","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1523/ENEURO.0020-25.2025","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
Excess Neonatal Testosterone Causes Male-Specific Social and Fear Memory Deficits in Wild-Type Mice.
Neurodevelopmental disorders disproportionately affect males compared with females. The biological mechanisms of this male susceptibility or female protection have not been identified. There is evidence that fetal/neonatal gonadal hormones, which play a pivotal role in many aspects of development, may contribute. Here, we investigate the effects of excess testosterone (T) during a critical period of sex-specific brain organization on social approach and fear learning behaviors in C57BL/6J wild-type mice. Male, but not female, mice treated with T on the day of birth (Postnatal Day 0; PN0) exhibited decreased social approach as juveniles and decreased contextual fear memory as adults, compared with vehicle (veh)-treated controls. These deficits were not driven by anxiety-like behavior or changes in locomotion or body weight. Mice treated with the same dose of T on PN18, which is outside of the critical period of brain masculinization, did not demonstrate impairments compared with the veh group. These findings indicate that excess T during a critical period of early development, but not shortly after, induces long-term deficits relevant to the male sex bias in neurodevelopmental disorders.
期刊介绍:
An open-access journal from the Society for Neuroscience, eNeuro publishes high-quality, broad-based, peer-reviewed research focused solely on the field of neuroscience. eNeuro embodies an emerging scientific vision that offers a new experience for authors and readers, all in support of the Society’s mission to advance understanding of the brain and nervous system.