Poster #13 - Childhood Adversity and the Neurodevelopment of Explicit Associative Learning

• In Event: 3-106 - Poster Session 11
  In Poster Session: PS 11 Section - Biological Processes: Neuroscience and Genetics

Integrative Statement

Background: Understanding how early exposure to adversity influences neurodevelopment is critical for identifying mechanisms that contribute to adverse life outcomes following childhood adversity. Few studies have examined how early adversity influences basic learning mechanisms and their underlying neural networks. We investigated whether childhood violence disrupts associative learning, which is a critical aspect of long-term episodic memory and relies on the hippocampus—a brain region that is sensitive to stress. Specifically, we examined whether childhood violence disrupted explicit associative learning and its neural correlates, whether deficits were broad or specific to threat-related cues, and whether these associations varied across development.

Hypothesis: We expected that violence-exposed children would exhibit poor associative memory and reduced hippocampal recruitment during encoding—specifically on trials involving angry faces—and that this pattern would not vary with age. Violence-exposed children have heightened attention to threatening faces (Pollak, 2003), which could limit visual processing of surrounding episodic details and interfere with hippocampus-dependent associative learning. Threat-specific associative learning deficits should emerge early in development and not vary with age given that heightened threat processing following violence begins as early as infancy (Cicchetti, 2005).

Methods: Children (n=60; 8-19 years, 24 violence-exposed) completed an explicit associative learning task with angry, happy, and neutral faces paired with objects during fMRI scanning. Outside the scanner, participants completed an associative memory test for face-object pairings.

Results: First, the association of violence with associative memory varied across development. Associative memory improved with age for control participants, but not for violence-exposed participants. Results did not vary as a function of the emotional nature of the stimuli being encoded. Second, left intraparietal sulcus (IPS) activation increased more with age for control participants than for violence-exposed participants, and predicted better associative memory. Right middle frontal gyrus (MFG) activation increased more with age for violence-exposed participants than for control participants, but was not associated with associative memory. Third, violence-exposed participants exhibited reduced hippocampal volume and activation during encoding, which mediated the association of violence with worse associative memory. This pattern did not vary by age or emotion type.

Conclusion: Children without exposure to violence exhibited better associative memory with increasing age as well as greater activation in the left IPS, which was associated with better associative memory. Violence-exposed participants exhibited no improvement in associative memory with age. Broad associative learning deficits in violence-exposed participants may become more pronounced with age due to under-recruitment of the parietal cortex and inefficient recruitment of the PFC. The parietal cortex and PFC increasingly support explicit memory across development (Ofen, 2012), and violence-exposed children exhibit reduced volume/thickness in these regions (Hanson, 2010). Reduced hippocampal volume and activation during encoding also explained the association of violence exposure with poor associative memory. Broad associative learning deficits may be a functional consequence of altered hippocampal structure and function following childhood violence, as hippocampal activation has been found to support explicit memory in children and adolescents (Ofen, 2012).

Authors

• Hilary Lambert, University of Washington
  Presenting Author

• Matt Peverill, University of Washington
  Non-Presenting Author

• Kelly Sambrook, University of Washington
  Non-Presenting Author

• Maya Rosen, University of Washington
  Non-Presenting Author

• Margaret Sheridan, University of North Carolina at Chapel Hill
  Non-Presenting Author

• Katie McLaughlin, Harvard University
  Non-Presenting Author