The day has finally come- I’m finally published and second author on a publication! Most of this work was done as part of my rotation project during my first year in graduate school. These findings (particularly the social behavior data) were my intellectual and technical contribution to the project and they laid the foundation for the NSF GRFP that I wrote in 2010 and was awarded in 2011. I’m extremely happy and proud to be able to share my personal line of research with all of you and I’d love to hear your questions/comments. Thanks for following and go click on the link above to read the full article!

Effects of Early-Life Abuse Differ across Development: Infant Social Behavior Deficits Are Followed by Adolescent Depressive-Like Behaviors Mediated by the Amygdala.

Raineki C, Cortés MR, Belnoue L, Sullivan RM.

Emotional Brain Institute, Nathan Kline Institute, Child Study Center, Child and Adolescent Psychiatry, New York University School of Medicine, Orangeburg, New York 10962.

Abuse during early life, especially from the caregiver, increases vulnerability to develop later-life psychopathologies such as depression. Although signs of depression are typically not expressed until later life, signs of dysfunctional social behavior have been found earlier. How infant abuse alters the trajectory of brain development to produce pathways to pathology is not completely understood. Here we address this question using two different but complementary rat models of early-life abuse from postnatal day 8 (P8) to P12: a naturalistic paradigm, where the mother is provided with insufficient bedding for nest building; and a more controlled paradigm, where infants undergo olfactory classical conditioning. Amygdala neural assessment (c-Fos), as well as social behavior and forced swim tests were performed at preweaning (P20) and adolescence (P45). Our results show that both models of early-life abuse induce deficits in social behavior, even during the preweaning period; however, depressive-like behaviors were observed only during adolescence. Adolescent depressive-like behavior corresponds with an increase in amygdala neural activity in response to forced swim test. A causal relationship between the amygdala and depressive-like behavior was suggested through amygdala temporary deactivation (muscimol infusions), which rescued the depressive-like behavior in the forced swim test. Our results indicate that social behavior deficits in infancy could serve as an early marker for later psychopathology. Moreover, the implication of the amygdala in the ontogeny of depressive-like behaviors in infant abused animals is an important step toward understanding the underlying mechanisms of later-life mental disease associated with early-life abuse.