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Targeted calretinin expression in granule cells of calretinin-null mice restores normal cerebellar functions Bertrand Bearzatto * , Laurent Servais * ,† , Céline Roussel * , David Gall * , Fawzia Baba-Aïssa * , Stéphane Schurmans ‡ , Alban de Kerchove d’Exaerde * , Guy Cheron † ,§ and Serge N. Schiffmann * ,1 * Laboratory of Neurophysiology, ‡ IRIBHM, IBMM, § Laboratory of Movement Biomechanics Université Libre de Bruxelles, Brussels, Belgium; and † Laboratory of Electrophysiology, Université Mons-Hainaut, Mons, Belgium 1 Correspondence: Laboratory of Neurophysiology CP601, Université Libre de Bruxelles, route de Lennik 808, Brussels 1070, Belgium. E-mail: sschiffm@ulb.ac.be <h3>SPECIFIC AIMS</h3> Inactivation of gene coding for calretinin, a calcium binding protein acting as a fast calcium buffer, deeply altered the cerebellar physiology leading to motor discoordination. Although mechanistic hypotheses have been proposed to explain these alterations, the widespread expression of calretinin in the whole central nervous system and its expression in several neuronal types in the cerebellar circuitry preclude a precise mechanistic demonstration. The aim of this study was to determine to what extent the expression of calretinin in a specific neuronal cell type, the cerebellar granule cells, contributes to the phenotype detected in calretinin knockout (Cr

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