Fetal Nicotine Exposure Increases Preference for Nicotine Odor in Early Postnatal and Adolescent, but Not Adult, Rats

Nicole M Mantella,Paul F Kent,Steven L Youngentob,John I Glendinning

doi:10.1371/journal.pone.0084989

Nicole M Mantella, Paul F Kent + Show 2 more

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https://doi.org/10.1371/journal.pone.0084989

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Journal: PloS one	Publication Date: Dec 17, 2013
Citations: 16	License type: CC BY 4.0

Affiliation: SUNY Upstate Medical University, Binghamton University

Abstract

Human studies demonstrate a four-fold increased possibility of smoking in the children of mothers who smoked during pregnancy. Nicotine is the active addictive component in tobacco-related products, crossing the placenta and contaminating the amniotic fluid. It is known that chemosensory experience in the womb can influence postnatal odor-guided preference behaviors for an exposure stimulus. By means of behavioral and neurophysiologic approaches, we examined whether fetal nicotine exposure, using mini-osmotic pumps, altered the response to nicotine odor in early postnatal (P17), adolescent (P35) and adult (P90) progeny. Compared with controls, fetal exposed rats displayed an altered innate response to nicotine odor that was evident at P17, declined in magnitude by P35 and was absent at P90 - these effects were specific to nicotine odor. The behavioral effect in P17 rats occurred in conjunction with a tuned olfactory mucosal response to nicotine odor along with an untoward consequence on the epithelial response to other stimuli – these P17 neural effects were absent in P35 and P90 animals. The absence of an altered neural effect at P35 suggests that central mechanisms, such as nicotine-induced modifications of the olfactory bulb, bring about the altered behavioral response to nicotine odor. Together, these findings provide insights into how fetal nicotine exposure influences the behavioral preference and responsiveness to the drug later in life. Moreover, they add to a growing literature demonstrating chemosensory mechanisms by which patterns of maternal drug use can be conveyed to offspring, thereby enhancing postnatal vulnerability for subsequent use and abuse.

Highlights

There are over 4000 different chemicals in inhaled cigarette smoke, nicotine is the addictive component and the key constituent responsible for the maintenance of tobacco product use (e.g.,[1])
Because the data set was multivariate, we performed a standard principle components analysis (PCA) on the entire data set in order to compress the deconstructed variables for each stimulus response of an animal into two uncorrelated values
In summary of our key neurophysiologic findings, we demonstrated that: (1) independent of maternal treatment the unique location of differential spatial activity for each odorant stimulus was comparable across all animals; (2) fetal nicotine exposure resulted in a stabilized magnitude of responsiveness and pattern distinctiveness in response to nicotine odor; and (3) fetal nicotine exposure resulted in an increase in responsivity and differential pattern muting in response to the non-exposure odorants

Summary

Introduction

There are over 4000 different chemicals in inhaled cigarette smoke, nicotine is the addictive component and the key constituent responsible for the maintenance of tobacco product use (e.g.,[1]). Rodent models of fetal nicotine exposure both parallel and predict findings from maternal smoking studies in humans Prenatal exposure via maternal smoking can cause a variety of behavioral changes. These include but are not limited to hyperactivity, impulsivity, and defects in learning, memory and attention [3,4,5,6,7]. These behavioral effects are in addition to retarded fetal growth, premature birth, stillbirths and increased mortality of newborn [8,9,10,11]

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