title: Emergence of social behavior deficit, blunted corticolimbic activity and adult depression-like behavior in a rodent model of maternal maltreatment.
abstract: Disrupted social behavior is a core symptom of multiple psychiatric and neurodevelopmental disorders. Many of these disorders are exacerbated by adverse infant experiences, including maltreatment and abuse, which negatively affect amygdala development. Although a link between impaired social behavior, abnormal amygdala function and depressive-like behavior following early adversity has been demonstrated in humans and animal models, the developmental emergence of maltreatment-related social deficits and associated amygdala neural activity are unknown. We used a naturalistic rodent model of maternal maltreatment during a sensitive period, postnatal days 8-12 (PN8-12), which produces social behavior deficits that precede adolescent depressive-like behavior and amygdala dysfunction, to examine social behavior in infancy, periweaning and adolescence. Neural activity in response to the social behavior test was assessed via c-Fos immunohistochemistry at these ages. A separate group of animals was tested for adult depressive-like behavior in the forced swim test. Maltreatment spared infant (PN16-18) social behavior but disrupted periweaning (PN20-22) and adolescent (PN42-48) social behavior. Maltreated rats exhibited blunted neural activation in the amygdala and other areas implicated in social functioning, including the medial prefrontal cortex and nucleus accumbens, at these ages and increased adult depressive-like behavior. These findings may suggest corticolimbic involvement in the emergence of maltreatment-induced social deficits that are linked to adult depressive-like behavior, thereby highlighting potential targets for therapeutic intervention. Understanding how infant experiences influence social behavior and age-specific expression across development may provide insights into basic neural mechanisms of social behaviors and disease-relevant social dysfunction exacerbated by early-life stress.
authors: Department of Child and Adolescent Psychiatry, Child Study Center, New York University Langone Medical Center, New York, NY, USA.|Neuroscience and Physiology, Sackler Institute for Graduate Biomedical Studies, New York University School of Medicine, New York, NY, USA.|Emotional Brain Institute, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, USA.
authors: M
authors: M
authors: Rincón-Cortés
authors: Department of Child and Adolescent Psychiatry, Child Study Center, New York University Langone Medical Center, New York, NY, USA.|Neuroscience and Physiology, Sackler Institute for Graduate Biomedical Studies, New York University School of Medicine, New York, NY, USA.|Emotional Brain Institute, Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, USA.
authors: R M
authors: RM
authors: Sullivan
mesh_terms: D000367:Age Factors; D000679:Amygdala / Q000503:physiopathology*; D000818:Animals; D002540:Cerebral Cortex / Q000503:physiopathology*; D003866:Depressive Disorder / Q000503:physiopathology*; D004195:Disease Models, Animal; D005260:Female; D015870:Gene Expression / Q000235:genetics; D008016:Life Change Events; D008297:Male; D016760:Proto-Oncogene Proteins c-fos / Q000235:genetics; D051381:Rats; D020318:Rats, Long-Evans; D012920:Social Behavior Disorders / Q000503:physiopathology*; D014886:Weaning
chemical_list: D016760:Proto-Oncogene Proteins c-fos