The bonding between mothers and their infants have critical long term impacts on the child's physical and mental well-being across lifespan. Thus the social and biological mechanisms that support optimal bonding are critical for the child's optimal development. Prior work from our team has shown that BOLD activation in the nucleus accumbens (NAcc) is related to the level of behavioral synchronization between a mother and an infant, which is taken to be an indicator of optimal bonding. Among mothers who are synchronous with their infants, the response of the NAcc to the infant is stronger than among non-synchronous mothers, and is correlated with oxytocin plasma levels. The NAcc, along with several other key structures, belong to our recently discovered social affiliation network;strength of intrinsic connectivity within this network is linked to greater social connectedness. Synthesizing these findings, we propose an innovative model by which mother- infant synchrony leads to a oxytocin-dependent dopamine release in the NAcc and other regions of the social affiliation network. In this R21 application, we plan to use an innovative multi-disciplinary method as we begin to explore this model and measure its four components: behavioral assessments of mother-infant synchrony, which is linked to oxytocin (that will be measured in the plasma), which in turn is linked to endogenous dopamine secretion and social affiliation neural network connectivity (measured by combined fMRI-PET imaging). Together, they will allow us to assess the extent to which the anatomy, intrinsic connectivity, and functional response in this social affiliation network is linked to synchrony in a way that is mediated by dopamine and oxytocin, which are key neurotransmitters in this network. Specifically, we plan to examine if mothers with stronger connectivity in the social affiliation network are more synchronous with their infants (Aim 1). We will also evaluate whether synchronous mothers have a greater BOLD response in this network when viewing a film of their own infant for 20 minutes vs. when viewing an unfamiliar infant (Aim 2). Moreover, we will evaluate whether infant-related stimuli enhance endogenous dopamine release and whether synchronous mothers will have greater endogenous dopamine release that is correlated to oxytocin, in response to their infants. We will also explore which regions in the social affiliation network show the greatest dopamine binding (Aim 3). Understanding the neurobiological mechanisms in the mother that promote successful bonding may significantly reduce the prevalence of childhood illness and increases the child's wellbeing. Additionally, the proposed research will establish that social reward is a mechanism for human maternal affiliation, and it will begin to parse apart the neurochemistry involved in this mechanism. Last, this study plan to use a novel research methodology of combined PET and fMRI in the functional study of human behavior, and to utilize it in favor of children's development.

Public Health Relevance

The mother-infant bond is critical for a child's physical and mental well-being across the lifespan. In this study, we begin to study the biological mechanisms that support this bond in humans. Understanding the neurobiological mechanisms in the mother that promote successful bonding will significantly reduce the prevalence of illness in the child's future, thus will have a range of social, medical and financial impacts.

Agency
National Institute of Health (NIH)
Institute
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Type
Exploratory/Developmental Grants (R21)
Project #
1R21HD076164-01A1
Application #
8633548
Study Section
Child Psychopathology and Developmental Disabilities Study Section (CPDD)
Program Officer
Freund, Lisa S
Project Start
2014-04-15
Project End
2016-03-31
Budget Start
2014-04-15
Budget End
2015-03-31
Support Year
1
Fiscal Year
2014
Total Cost
Indirect Cost
Name
Massachusetts General Hospital
Department
Type
DUNS #
City
Boston
State
MA
Country
United States
Zip Code
02199
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