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Human Molecular Genetics, 2002, Vol. 11, No. 21 2567-2580
© 2002 Oxford University Press

Deletion of the mental retardation gene Gdi1 impairs associative memory and alters social behavior in mice

Patrizia D'Adamo1,2, Hans Welzl2, Stavros Papadimitriou1, Marina Raffaele di Barletta1, Cecilia Tiveron3, Laura Tatangelo3, Laura Pozzi3, Paul F. Chapman4, Simon G. Knevett5, Mark F. Ramsay4, Flavia Valtorta5, Chiara Leoni5, Andrea Menegon5, David P. Wolfer2, Hans-Peter Lipp2 and Daniela Toniolo1,5,*

1Institute of Genetics Biochemistry and Evolution–CNR, Pavia, Italy, 2Institute of Anatomy, University of Zurich, Zurich, Switzerland, 3Centro Ricerca Sperimentale, Istituto Regina Elena, Roma, Italy, 4Cardiff School of Biosciences, Cardiff University, Cardiff, UK and 5San Raffaele Scientific Institute, Milano, Italy

Received April 10, 2002; Accepted July 5, 2002

Non-specific mental retardation (NSMR) is a common human disorder characterized by mental handicap as the only clinical symptom. Among the recently identified MR genes is GDI1, which encodes {alpha}Gdi, one of the proteins controlling the activity of the small GTPases of the Rab family in vesicle fusion and intracellular trafficking. We report the cognitive and behavioral characterization of mice carrying a deletion of Gdi1. The Gdi1-deficient mice are fertile and anatomically normal. They appear normal also in many tasks to assess spatial and episodic memory and emotional behavior. Gdi1-deficient mice are impaired in tasks requiring formation of short-term temporal associations, suggesting a defect in short-term memory. In addition, they show lowered aggression and altered social behavior. In mice, as in humans, lack of Gdi1 spares most central nervous system functions and preferentially impairs only a few forebrain functions required to form temporal associations. The general similarity to human mental retardation is striking, and suggests that the Gdi1 mutants may provide insights into the human defect and into the molecular mechanisms important for development of cognitive functions.

* To whom correspondence should be addressed at: IGBE–CNR, Via Abbiategrasso 207, 27100 Pavia, Italy. Tel: +39 0382546340; Fax: +39 0382422286; Email: toniolo{at}igbe.pv.cnr.it


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