Maya Opendak, Emotional Brain Institute, Nathan Kline Institute & Department of Child and Adolescent Psychiatry, New York University School of Medicine, New York, USA
Previous research has identified correlations between early-life trauma and maladaptive outcomes, but the developmental mechanisms initiating the pathway to pathology remain elusive. Using two complementary rodent models of infant trauma with a caregiver, we observed an attenuation of infant neurobehavioral attachment responses to the maternal odor over time. Whereas maternal presence buffered the effects of acute trauma (shock) on pups’ amygdala activation, ultrasonic vocalizations, and HPA response, repeated trauma in the presence of the mother led to reversal of these buffering effects and long-term neurobehavioral impairments. After five days of trauma with the mother, pups exhibited blunted amygdala response to the maternal odor as well as impaired attachment behaviors towards her in a social test. This was accompanied by changes in amygdala structure and function, including neurogenesis, DNA methylation, and expression of c Fos and D1 receptors. Furthermore, pups shocked with the mother showed an increase in amygdala dopamine, a reversal of the decrease observed in pups shocked alone. Blockade of amygdala dopamine during trauma with the mother restored typical attachment behavior. Taken together, these data suggest that the effects of early-life abuse may involve devaluation of the caregiver and dopamine may provide a novel therapeutic target for infant abuse.
FUNDING: This work was supported by National Institutes of Health grants MH100123 (MO), R01MH115914 (KGB) and NIH DP5 Early Independence Award and BBRF/NARSAD Young Investigator Award (DG).