Presenter: Emilee McDonald – Biology
Faculty Mentor(s): Adrianne Huxtable, Robyn Naidoo
Session: (In-Person) Poster Presentation
An understudied population in the opioid crisis are infants exposed to maternal opioids experiencing breathing deficits. Our animal model of maternal opioids demonstrated neonatal breathing deficits after birth, which normalized with age despite continued maternal opioid exposure, suggesting neonatal compensation to this early life opioid stressor. To understand the mechanisms of these breathing deficits, we tested the hypothesis that maternal opioids decrease opioid receptor expression (since opioids activate opioid receptors to exert their effects) in a key brainstem site for breathing. Brainstem immunohistochemistry and confocal microscopy assessed typical developmental changes in neonatal opioid receptor expression after maternal no treatment (control). Opioid receptor expression was highest at postnatal day 0 (P0), when neonates begin breathing, and decreased through P11, a critical maturation period of the nervous system. In neonates after maternal opioids, opioid receptor expression was evaluated at P0 (birth), P4 when neonates still receive opioids through breast milk, and P11 after opioid exposure has ceased. Preliminary data support decreased opioid receptor expression in P0 and P4 neonates after maternal opioids, but a return to control levels at P11. Thus, maternal opioids acutely impair opioid receptor expression in a brainstem site critical for breathing, suggesting opioid receptors may be key to neonatal breathing impairments after maternal opioid exposure.