Postnatal effects of prenatal nicotine exposure on body weight, brain size and cortical connectivity in mice.

Maternal smoking results in myriad physical, cognitive, and behavioral effects in offspring due to prenatal exposure to nicotine. As the mammalian neocortex coordinates sensory integration and higher-order processes including cognition and behavioral regulation, it follows that cognitive and behavioral phenotypes of prenatal nicotine exposure (PNE) may correlate with, or stem from changes in anatomy and physiology of the neocortex. The current study uses a prenatal nicotine mouse model to determine effects of PNE on body weight, brain weight, brain length and development of neocortical circuitry, including thalamocortical afferents (TCAs) and intraneocortical connections (INCs). Although dam nutrition, dam weight gain and litter size were not significantly affected by nicotine treatment, PNE resulted in lower newborn birth weight, brain weight and length. Interestingly, the reduction of body weight, brain weight, and brain length observed in newborn PNE mice compared to control mice was no longer present at postnatal day (P) 10. A morphological study of somatosensory and visual TCAs and INCs shows no major defects in areal patterning of these connections. These data add to a growing body of literature on the neurobiological effects of PNE by providing new information on the time course of PNE-related change in the postnatal brain.