A National Research Priority Program of  
the

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Funding Period 2011 - 2013

P5

Glutamatergic contributions to nicotine-induced cognitive enhancement (HU1302/2-2)

Dr. René Hurlemann (Principle Investigator)
University of Bonn
Dept. of Psychiatry
Sigmund-Freud-Str. 25

53127 Bonn
+49-228-287-15057
rene.hurlemann(at)ukb.uni-bonn.de

 

 

Project group:

Neuromodulation of Emotion (NEMO) Research Group

Department of Psychiatry

University of Bonn

53105 Bonn

Germany

URL: http://web.me.com/renehurlemann/Website/Welcome.html

 

Together with

 

Yoan Mihov, MSc

Department of Psychiatry

University of Bonn

53105 Bonn

Germany

Yoan.Mihov(at)ukb.uni-bonn.de

 

Project partners:

 

Prof. Dr. N.J. Shah
Institute of Neuroscience and Medicine (INM-4)
Research Center Juelich
52425 Juelich

+49-2461-61-6836
Fax: +49-2461-61-1919
n.j.shah(at)fz-juelich.de

 

Prof. Dr. Andreas Bauer

Institute of Neuroscience and Medicine (INM-2)
Molecular Organisation of the Human Cortex
Research Center Juelich
52425 Juelich
+49-2461-61-4288
Fax: +49-2461-61-2820
an.bauer(at)fz-juelich.de

 

Whereas our previous clinical project (“The effects of gender and nicotine addiction on human amygdala function in social interaction“, HU1302/2-1) was designed to investigate the structural and functional integrity of the amygdala in chronic smokers, the present preclinical project is focused on the acute influence of nicotine on amygdala-hippocampal learning in nonsmokers. Accumulating evidence implicates nicotine in cognitive enhancement, with facilitating effects on learning observed even after single-dose administration. However, the molecular mechanisms underlying these cognitive-enhancing effects of nicotine are little understood. Animal studies suggest that administration of nicotine could augment amygdala-hippocampal learning through cholinergic-glutamatergic interactions via nicotinic acetylcholine receptors (nAChR) and Nmethly-D-aspartate receptors (NMDAR). To specifically test this hypothesis in humans, the present project combines functional magnetic resonance imaging (fMRI) with probabilistic mapping of amygdalar and hippocampal subregions to precisely localize a nicotine-induced enhancement of learning. If the facilitating effects of nicotine on learning require cholinergic-glutamatergic interactions via nAChR and NMDAR, then these effects should be blocked by the NMDAR antagonist memantine and potentiated by the NMDAR partial agonist D-cycloserine. A potentiation of amygdala-hippocampal learning following co-administration of nicotine and D-cycloserine would significantly inform novel strategies of cognitive enhancement in patient populations and healthy people.