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First published online 27 January 2009
doi: 10.1242/jcs.033464
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Research Article |
1 INMED/INSERM U29, Parc Scientifique de Luminy, 13273, Marseille, France
2 INSERM U 751, Université d'Aix-Marseille, Hôpital de la Timone, Marseille, France
3 Department of Neurobiology and Behavior, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan
4 CNRS UMR 6184, Neurobiologie des Interactions Cellulaires et Neurophysiopathologie (NICN), IFR Jean Roche, Marseille, F-13020, France
* Author for correspondence (e-mail: lotfi.ferhat{at}univmed.fr)
Accepted 30 October 2008
Drebrin A, one of the most abundant neuron-specific F-actin-binding proteins, is found exclusively in dendrites and is particularly concentrated in dendritic spines receiving excitatory inputs. We investigated the role of drebrin A in synaptic transmission and found that overexpression of drebrin A augmented the glutamatergic synaptic transmission, probably through an increase of active synaptic site density. Interestingly, overexpression of drebrin A also affected the frequency, amplitude and kinetics of miniature inhibitory postsynaptic currents (mIPSCs), despite the fact that GABAergic synapse density and transmission efficacy were not modified. Downregulation of drebrin A led to a decrease of both glutamatergic and GABAergic synaptic activity. In heterologous cells, drebrin A reorganized and stabilized F-actin and these effects were mediated by its actin-binding domain. Thus, drebrin A might regulate dendritic spine morphology via regulation of actin cytoskeleton remodeling and dynamics. Our data demonstrate for the first time that drebrin A modulates glutamatergic and GABAergic synaptic activities.
Key words: Spine morphogenesis, F-actin, GABA, Glutamate, vGlut1, Gad-65, Bassoon
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