EPIGENETIC RISK FOLLOWING EARLY LIFE STRESS IN INFANT RHESUS MACAQUES

这个子项目是利用这些资源的众多研究子项目之一

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. The experience of early life stress puts individuals at greater risk for psychopathology later in life. Multiple neural pathways contribute to this risk, but the serotonin transporter (5-HTT) is among the foremost of these. The target of the most effective antidepressants, neural 5-HTT expression is lower in depressed patients and in victims of early life stress. Identifying the mechanism(s) of plasticity in 5-HTT gene function or of its transcription factors following early stress may therefore inform intervention strategies to improve mental health following trauma. The PI will investigate whether a well-characterized experimental early life stressor leads to dysregulation of 5-HTT and one of its major transcriptional enhancers(glucocorticoid receptor, NR3C1 or GR) in infant rhesus macaques, and whether this dysregulation is epigenetically mediated.