A new study sheds light on changes in the brain that may explain why young infants who are placed in an orphanage or foster care often struggle with social relationships later in life.
The findings, which were published in the journal Developmental Psychobiology, come from a team of researchers led by Julie Fudge, M.D., with the University of Rochester Medical Center (URMC) Department of Neuroscience. The scientists revisited data from a study involving monkeys that took place more than a decade ago at the University of Pittsburgh and was designed to observe the behaviors of newborns that were separated from their biological mothers and raised by another group of females. The original study noted that these monkeys differed in their social interactions – such as grooming, huddling together, and normal aggression – compared to those that were raised by their mothers.
Like humans, monkey’s brains are not fully developed at birth and the animals are dependent upon the nurturing of caregivers for many months early in life. Fudge and her colleagues wanted to see if there could find an association between the absence of a primary caregiver and biological changes in the brain that could explain the lasting social impairment observed in the monkeys.
The researchers focused on a specific region of the brain called the amygdala, which is known to be important for social and emotional development and behaviors. Infancy is a critical stage for the development of the amygdala as it harbors a population of immature nerve cells that are essentially awaiting instructions.
Using brain tissue that had been long preserved from the original study, the researchers identified a specific gene, called tbr1, which was essentially switched off in the amygdala of monkeys that were raised in an environment without their biological mothers. This lower expression of tbr1 was associated with less time spent by the infants engaging typical social behaviors. While the tbr1 gene is known to play a role in prenatal brain development and has also been associated with autism, a condition characterized by impaired social development, this is the first time it had been identified as playing a key role in brain development after birth.
The scientists are not entirely sure what causes this gene to become inactive, but speculate that it may be triggered, in part, by inputs from one’s environment. For example, the absence of intense social and sensory stimulation or cues from a primary caregiver or the stress of separation could suppress the expression of tbr1, causing the immature cells in the amygdala to either develop more slowly or fail to effectively integrate into the brain’s networks of circuits, resulting in developmental delays.
The researchers believe the findings show clear evidence that in higher primates, there are key brain regions that continue neural development in infancy and that environmental interaction can influence the growth, formation, and integration of cells in the amygdala in the early months of life.
Additional co-authors of the study include Danielle de Campo and Joseph Miano with URMC, Judy Cameron and David Lewis the University of Pittsburgh, and Karoly Mirnics with University of Nebraska. The research was supported with funding from grants from the National Institutes of Mental Health, Clinical and Translational Science Research Pilot Award, and the John D. and Catherine T. McArthur Foundation Network on Early Experience and Brain Development.