It has been recognized that the foundation of most, if not all, complex disease processes, particularly neuropsychiatric disorders, is due to the interactions between subtle genetic deficits and environmental insults. One of the most studied neuropsychiatric disorders shown to contribute from both heritable-related factors and environmental stressor sensitivity is Attention Deficit Hyperactivity Disorder (ADHD). Of the heritable issues involved, meta-analysis of genetic linkage studies has shown that the SNARE protein SNAP-25, is one of many possible proteins that may provide answers to the genetic component. In contrast to this genetic factor, studies have shown that prenatal nicotine exposure causes a direct effect to the fetus and predisposes them to nicotine and substance abuse behavior. Finally, preliminary studies have shown that heterozygote SNAP-25 deficient mice following in-utero exposure to nicotine are, in fact, hyperactive compared to their wild type littermates. To study the relationship between SNAP-25 and prenatal nicotine exposure with locomotor activity, we compared wild type mice with and without nicotine exposure to SNAP-25 wild type mice with and without nicotine exposure. Additionally, this study also examined prenatal nicotine exposed SNAP-25 heterozygous mice with their wild type counterpart with intraperitoneal cocaine to see if the combination of factors increased the likelihood of substance abuse potential. The results demonstrated that prenatal nicotine exposed mice had greater locomoter activity and substance abuse behavior. Moreover the SNAP-25 heterozygous genotype compounded both of these affects and demonstrated greater results.
Adcock, Jarrod; Michaela Haney; D. Leonard; and Andrea Allan. "The Effects of SNAP-25 Deficits and Pre-Natal Nicotine in a Mouse and ADHD Model." (2009). https://digitalrepository.unm.edu/ume-research-papers/52