Funding Period 2011 - 2013
P12
Schizophrenia and Nicotine Addiction: Analysis of genetic mouse models (ZI 361/7-1)
Prof. Dr. Andreas Zimmer (Principle Investigator)
Institute of Molecular Psychiatry
University of Bonn
Sigmund Freud Str. 25
53127 Bonn
+49-228-6885-300
Fax: +49-228-6885-301
Neuro(at)uni-bonn.de
Together with:
PD Dr. A. Bilkei-Gorzo
Institute of Molecular Psychiatry
University of Bonn
Sigmund-Freud-Str. 25
53127 Bonn
+49-228 - 6885-317
Fax: +49-228 - 6885-301
abilkei(at)uni-bonn.de
Dr. Boris Hambsch
Institute of Molecular Psychiatry
University of Bonn
Sigmund-Freud-Str. 25
53127 Bonn
+49-228 - 6885-320
Fax: +49-228 - 6885-301
hambsch(at)uni-bonn.de
Dr. Xavier Miro
Institute of Molecular Psychiatry
University of Bonn
Sigmund-Freud-Str. 25
53127 Bonn
+49-228 - 6885-334
Fax: +49-228 - 6885-301
xmiro(at)uni-bonn.de
Dr. Eva Drews
Institute of Molecular Psychiatry
University of Bonn
Sigmund-Freud-Str. 25
53127 Bonn
+49-228 - 6885-306
Fax: +49-228 - 6885-301
Edrews(at)uni-bonn.de
Prof. Dr. Michael Wagner (Project partner)
Experimentelle und Klinische Neuropsychologie
Psychiatrische Klinik der Universität Bonn
Sigmund-Freud-Str. 25
53105 Bonn
+49-228-287-16377
Michael.Wagner(at)ukb-bonn.de
It has been recognized for many years that a disproportionally high percentage of schizophrenic patients smoke. A worldwide meta-analysis of smoking and schizophrenia revealed a 3-6 times greater smoking incidence in schizophrenic patients compared to the general population and twice the incidence compared with other major mental illnesses. In addition, schizophrenic patients smoke cigarettes much more intensively and have more difficulties to quit smoking.
This project addresses the molecular mechanisms that contribute to the high comorbidity of schizophrenia and nicotine addiction, by investigating the effect of nicotine in animal models with a deletion or transgenic over-expression of schizophrenia risk genes. We hypothesize that schizophrenic patients consume nicotine as a form of self-medication. Thus, acute and chronic nicotine administration might have beneficial effects on the behavioural deficits in paradigms for schizophrenia-like symptoms that have been observed in the genetic mouse models. Our alternative, not mutually exclusive, hypothesis is that the rewarding and/or addictive properties of nicotine are enhanced in genetic models of schizophrenia. This hypothesis will be tested by assessing the rewarding properties of nicotine in different behavioral paradigms. Further we will assess somatic signs of nicotine withdrawal after chronic administration. We will start to evaluate the molecular mechanisms that contribute to the anticipated differential effects of nicotine in these mouse models, by assessing nicotine receptor levels and downstream signalling pathways.