Original Article
Neuropsychopharmacology (2007) 32, 693–699. doi:10.1038/sj.npp.1301066; published online 22 March 2006
Behavioral Teratogenicity Induced by Nonforced Maternal Nicotine Consumption
Rodrigo Paz1,2,3, Brigg Barsness4, Trevor Martenson4, Daniel Tanner1 and Andrea M Allan1
- 1Department of Neurosciences, University of New Mexico, Albuquerque, NM, USA
- 2Departamento de Psiquiatría y Neurociencias, Universidad Diego Portales, Portales, Chile
- 3Instituto Psiquiátrico Dr José Horwitz Barak, Santiago de Chile, Chile
- 4School of Medicine, University of New Mexico, Albuquerque, NM, USA
Correspondence: Dr AM Allan, Department of Neurosciences, University of New Mexico, Albuquerque, NM 87131-0001, USA. Tel: +1 505 272 8811, Fax: +1 505 272 8082, E-mail: aallan@salud.unm.edu
Received 27 December 2005; Revised 3 February 2006; Accepted 9 February 2006; Published online 22 March 2006.
Abstract
Prenatal nicotine exposure (PNE) has been associated with increased prevalence of attention deficit hyperactivity disorder (ADHD), major depressive disorder (MDD) and substance abuse in exposed children and adolescents. Whether these syndromes are caused by nicotine exposure, or genetic and psychosocial adversities associated with maternal smoking is not completely clear. Animal models suggest a direct impact of PNE. However, the fact that nicotine is forcefully administrated in these paradigms raises some questions about the specificity of these findings. Pregnant C57BI/6J mice were allowed to choose drinking saccharin/nicotine solutions or pure water. Controls could choose saccharin solutions or pure water. Offspring were tested in spontaneous locomotion, fear-associated learning (trace conditioning), addictive (conditioned place preference), and depression-like (learned helplessness) behaviors. There was no significant difference in weight or pup number between the prenatal treatment groups. A significant effect of PNE was observed on spontaneous locomotion, preference for a cocaine-associated place, and latency to escape in the learned helplessness paradigm. Surprisingly, PNE mice exhibited an increased learning of trace-conditioned fear-associated cues. The hyperlocomotive behavior reported in animal models of PNE is not likely an artifact of forceful nicotine administration. The increased prevalence of ADHD, MDD and substance abuse observed in PNE children and adolescents is probably caused by direct behavioral teratogenic effects of PNE. The role of PNE as a risk factor of syndromes associated to increased learning of fear-associated cues such as post-traumatic stress disorder (PTSD) warrants further evaluation.
Keywords:
prenatal, nicotine, ADHD, substance abuse, PTSD, depression
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