Infants in the Neonatal Intensive Care Unit (NICU) regularly experience tissue damage as part of their essential medical care.  Growing clinical and preclinical evidence indicates that such injuries not only cause acute pain but can also ‘prime’ developing nociceptive pathways and thereby persistently enhance pain perception following prolonged noxious stimulation later in life.  However, infants in the NICU are exposed to a variety of early life adversities beyond tissue damage, including chronic stress as well as iron deficiency that commonly accompanies premature birth.  Here Dr. Baccei will summarize recent preclinical work using mouse models to investigate the consequences of chronic stress during the neonatal period, or early life iron deficiency, on nociceptive processing at distinct stages of postnatal development.  He will present data to suggest that either neonatal stress or early life iron deficiency is sufficient to evoke short- and long-term effects on pain sensitivity, which include priming nociceptive circuits to respond more robustly to select types of injury sustained during adulthood.  Dr. Baccei will also discuss ongoing studies designed to reveal the potential cellular and molecular mechanisms by which such early life adversities can persistently shape nociceptive processing in the peripheral and central nervous systems.