Abstract

The study of neural-glial interactions within the brain is in its infancy.  However, there is mounting evidence that microglia and astrocytes, the primary immunocompetent cells of the CNS , are involved in every major aspect of brain development and function, including neurogenesis and migration, synaptic formation and pruning, and phagocytosis of apoptotic debris.  Many cytokines and chemokines (e.g., interleukin [IL]-1β and CCL2 , respectively) are produced by glia at much higher baseline levels in the developing brain compared to the adult brain, although this time course depends highly on brain region and sex. These collective data have led us to hypothesize that early development represents a sensitive period for immune perturbation and thus long-term alterations in neural function, because the immune system is so active within the brain at this time. Indeed, evidence from both animal and human studies implicates the immune system in a number of disorders with known or suspected developmental origins.  This talk will focus on the evidence that diverse challenges (e.g., infection, toxins, maternal stress) during distinct stages of development act as a vulnerability factor for later-life alterations in central immune signaling, and marked changes in behavior throughout the remainder of the lifespan, with a focus on the hypothesis that long-term changes in microglial cell function may underlie such vulnerability.

http://dibs.duke.edu/research/profiles/47-staci-bilbo http://www.neuro.duke.edu/training-faculty