Long-term alterations to dendritic morphology and spine density associated with prenatal exposure to nicotine

Prenatal exposure to nicotine has been associated with many long-term cognitive and behavioral abnormalities. Based upon these observable outcomes, we hypothesized that prenatal nicotine exposure would induce lasting changes in dendritic morphology and synaptic connectivity throughout the cortex. Pregnant Long-Evans rats were administered nicotine or saline for the duration of pregnancy and offspring were sacrificed at P100 for Golgi-Cox analysis (dendritic length, dendritic branching, and spine density) of the prefrontal cortex (AID and Cg3), parietal cortex, and nucleus accumbens. In male offspring dendritic branching increased in AID and NAc, but decreased in the apical field of Cg3; spine density increased everywhere except NAc where it decreased; and dendritic length was increased in Cg3basilar and NAc but reduced in PARbasilar. In female offspring, dendritic branching increased in NAc but decreased in AID; spine density increased in AID and PAR but decreased in Cg3 and NAc, and dendritic length was reduced in Cg3, PAR, and NAc. As changes were identified at P100, prenatal exposure to nicotine dramatically reorganized neuroanatomy in a persistent manner, likely altering the brain's response to normal and abnormal experiences.

► Prenatal nicotine exposure altered dendritic morphology and synaptic connectivity. ► Anatomical measures included dendritic branching, length, and spine density. ► Changes were identified on P100 in Cg3, AID, PAR1, and NAc. ► Sex dependent changes were noted in AID, Cg3, and NAc. ► Prenatal exposure to nicotine induces persistent neuroanatomical changes.