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Human Molecular Genetics Advance Access published online on August 7, 2006
Human Molecular Genetics, doi:10.1093/hmg/ddl206
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© The Author 2006. Published by Oxford University Press. All rights reserved
Received June 15, 2006
Revised July 28, 2006
Accepted July 28, 2006

Article

Monoamine Oxidase A-Knockout Mice Exhibit Impaired Nicotine Preference but Normal Responses to Novel Stimuli

Soh Agatsuma 1, MoonSook Lee 1, Hongwen Zhu 2, Kevin Chen 3, Jean Shih 3, Isabelle Seif 4, and Noboru Hiroi 5 *

1 Department of Psychiatry and Behavioral Sciences, Albert Einstein College of Medicine, Bronx, NY 10461, USA
2 Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461, USA
3 Department of Cell and Neurobiology, Keck School of Medicine, University of Southern California, Zonal Avenue, Los Angeles, CA 90089-9121 USA
4 Faculty of Pharmacy, University of Paris-Sud, 92296 Chatenay-Malabry, France
5 Laboratory of Molecular Psychobiology, Department of Psychiatry and Behavioral Sciences, Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA

* To whom correspondence should be addressed.
Noboru Hiroi, E-mail: hiroi{at}aecom.yu.edu


  Abstract

Nicotine is thought to act on brain monoamine systems that normally mediate diverse motivational behaviors. How monoamine-related genes contribute to behavioral traits (e.g., responses to novel stimuli) comorbid with the susceptibility to nicotine addiction is still poorly understood. We examined the impact of constitutive monoamine oxidase A (MAOA) deficiency in mice on nicotine reward and responses to novel stimuli. Age-matched, male Maoa-knockout (KO) mice and wild-type (WT) littermates were tested for nicotine-induced conditioned place preference (CPP); voluntary oral nicotine preference/intake; spontaneous locomotor activity in a novel, inescapable open field; and home-cage novel place preference. Nicotine preference in WT mice was reduced in Maoa-KO mice in the CPP and oral preference/intake tests. Control experiments showed that these phenotypes were not due to abnormalities in nicotine metabolism, fluid intake, or response to taste. By contrast, Maoa-KO mice were normal in their behavioral response to a novel, inescapable open field and in their preference for a novel place. The observed phenotypes suggest that a constitutive deficiency of MAOA reduces the rewarding effects of nicotine without altering behavioral responses to novel stimuli in mice. Constitutive MAOA activity levels are likely to contribute to the vulnerability or resiliency to nicotine addiction by altering the rewarding effects of nicotine.


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