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First published online October 12, 2006
doi: 10.1242/10.1242/jcs.03194
Research Article |
1 Center of Neuroscience and Neuroengineering, Department of Experimental Medicine, University of Genoa, Italy
2 Department of Cellular and Molecular Physiology and Pharmacology, University of Pavia, Italy
3 San Raffaele Scientific Institute, `Vita Salute' University and I.I.T. Unit of Molecular Neuroscience, Milan, Italy
4 Center of Excellence for Biomedical Research, University of Genoa, Italy
5 Unit of Neuroscience, The Italian Institute of Technology, Morego Central Laboratories, Genoa, Italy
Author for correspondence (e-mail: benfenat{at}unige.it)
Accepted 26 July 2006
Synapsins are synaptic-vesicle-associated phosphoproteins implicated in the regulation of neurotransmitter release and excitability of neuronal networks. Mutation of synapsin genes in mouse and human causes epilepsy. To understand the role of the highly conserved synapsin domain E in the dynamics of release from mammalian inhibitory neurons, we generated mice that selectively overexpress the most conserved part of this domain in cerebellar Purkinje cells. At Purkinje-cell–nuclear-neuron synapses, transgenic mice were more resistant to depression induced by short or prolonged high-frequency stimulations. The increased synaptic performance was accompanied by accelerated release kinetics and shorter synaptic delay. Despite a marked decrease in the total number of synaptic vesicles, vesicles at the active zone were preserved or slightly increased. The data indicate that synapsin domain E increases synaptic efficiency by accelerating both the kinetics of exocytosis and the rate of synaptic vesicle cycling and decreasing depression at the inhibitory Purkinje-cell–nuclear-neuron synapse. These effects may increase the sensitivity of postsynaptic neurons to inhibition and thereby contribute to the inhibitory control of network activity.
Key words: Synaptic vesicle release, Exocytosis, Synapsin, Synaptic plasticity, Cerebellum, Transgenic
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