Bringing basic research on early experience and stress neurobiology to bear on preventive interventions for neglected and maltreated children
A major focus in developmental psychopathology is on understanding developmental mechanisms and, armed with this information, intervening to improve children's outcomes. Translational research attempts to bridge the distance between understanding and intervention. In the collaborations that have formed the core of our research network on early experience, stress, and prevention science, we have focused on translating basic research on early experiences and stress neurobiology into preventive interventions for neglected and abused children. Our experiences in attempting to move from bench to bedside have led us to recognize the many challenges that face translational researchers. This review provides a brief synopsis of the animal model literature on early experience and stress neurobiology from which we glean several key bridging issues. We then review what is currently known about the impact of childhood neglect and abuse on stress neurobiology in human adults and children. Next, we describe how this work has informed the evaluation of our preventive interventions with maltreated children. Finally, we discuss several considerations that should facilitate a more complete integration of basic research on early experience and stress neurobiology into preventive intervention strategies. a
c1 Address correspondence and reprint requests to: Megan R. Gunnar, Institute of Child Development, 51 East River Road, University of Minnesota, Minneapolis, MN; E-mail: firstname.lastname@example.org
a This paper reflects the work of the Early Experience, Stress and Prevention Science Network (R21 MH65046), whose members are Mary Dozier, Philip Fisher, Nathan Fox, Megan Gunnar, Seymour Levine, Charles Neal, Seth Pollak, Paul Plotsky, Mar Sanchez, and Delia Vazquez. Preparation of this manuscript was supported by a Senior Scientist Award (K05 MH66208) to Megan Gunnar, and by MH59780 and MH65046, NIMH, U.S. PHS; MH46690, NIMH and ORMH, U.S. PHS; and DA17592, NIDA, NIH, U.S. PHS to Philip Fisher.