Nearly one third of women of reproductive age in the United States are prescribed opioids annually; 14% of women fill an opioid prescription during pregnancy, and one in five report misuse. As a result, there is an increasing population of infants born with gestational opioid exposure. During typical brain development, endogenous opioids and their receptors are highly expressed by neural progenitor cells, neurons, and glia where they modulate cell proliferation, differentiation, and maturation. Thus, any disruption to the endogenous opioid system during the critical period of brain development, such as exogeneous opioid exposure, would likely have lasting consequences on brain cell populations and the behaviors they influence. Indeed, opioid-exposed infants have smaller brains and show significant neurodevelopmental impairment as well as higher rates of learning disability at school age. To characterize how exposure to exogenous opioids during brain development affects neural cell maturation and cognitive performance, our lab has developed a clinically relevant rat model of perigestational morphine exposure. We report that perigestational morphine delays postnatal neuronal maturation, alters astrocyte and oligodendrocyte proliferation, and decreases expression of the neural growth factor BDNF in the hippocampus, a brain region critical for learning and memory. Behavioral assessments reveal selective impairment of spatial learning as measured by the Barnes Maze without significantly impacting memory or cognitive flexibility. Furthermore, we show that environmental enrichment can rescue the immature hippocampal BDNF profile and spatial learning deficits in males but not females, indicating the effectiveness of non-pharmacological and non-invasive interventions following gestational opioid exposure.