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• W2912808859 abstract "The ontogeny of antisocial behavior (ASB) is rooted in complex gene-environment (G×E) interactions. The best-characterized of these interplays occurs between: a) low-activity alleles of the gene encoding monoamine oxidase A (MAOA), the main serotonin-degrading enzyme; and b) child maltreatment. The purpose of this study was to develop the first animal model of this G×E interaction, to help understand the neurobiological mechanisms of ASB and identify novel targets for its therapy. Maoa hypomorphic transgenic mice were exposed to an early-life stress regimen consisting of maternal separation and daily intraperitoneal saline injections and were then compared with their wild-type and non-stressed controls for ASB-related neurobehavioral phenotypes. Maoa hypomorphic mice subjected to stress from postnatal day (PND) 1 through 7 – but not during the second postnatal week - developed overt aggression, social deficits and abnormal stress responses from the fourth week onwards. On PND 8, these mice exhibited low resting heart rate - a well-established premorbid sign of ASB – and a significant and selective up-regulation of serotonin 5-HT2A receptors in the prefrontal cortex. Notably, both aggression and neonatal bradycardia were rescued by the 5-HT2 receptor antagonist ketanserin (1–3 mg kg−1, IP), as well as the selective 5-HT2A receptor blocker MDL-100,907 (volinanserin, 0.1–0.3 mg kg−1, IP) throughout the first postnatal week. These findings provide the first evidence of a molecular basis of G×E interactions in ASB and point to early-life 5-HT2A receptor activation as a key mechanism for the ontogeny of this condition. This article is part of the Special Issue entitled ‘The neuropharmacology of social behavior: from bench to bedside’." @default.
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• W2912808859 date "2019-11-01" @default.
• W2912808859 modified "2023-10-10" @default.
• W2912808859 title "Gene-environment interactions in antisocial behavior are mediated by early-life 5-HT2A receptor activation" @default.
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• W2912808859 doi "https://doi.org/10.1016/j.neuropharm.2019.01.028" @default.
• W2912808859 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7578912" @default.
• W2912808859 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30716416" @default.
• W2912808859 hasPublicationYear "2019" @default.
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