Abstract
Because GABA (γ-aminobutyric acid) receptor-mediated inhibition controls the excitability of principal neurons in the brain, deficits in GABAergic inhibition have long been favored to explain seizures. In an experimental model of temporal lobe epilepsy, we have identified a deficit of inhibition in presynaptic GABAergic terminals characterized by decreased GABA quantal activity associated with reduced synaptic vesicle density. This decrease in vesicle number primarily seems to affect the reserve pool, rather than the docked or the readily releasable pool.
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Acknowledgements
Supported by INSERM-FIS and Fondation Simone et Cino del Duca. We thank D. Diabira for providing lesioned animals and H. Bellen, G. Buzsáki and A. Triller for comments on the manuscript. We are grateful to R. Cossart for performing blind statistical analysis on pooled electrophysiological and morphological data.
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Hirsch, J., Agassandian, C., Merchán-Pérez, A. et al. Deficit of quantal release of GABA in experimental models of temporal lobe epilepsy. Nat Neurosci 2, 499–500 (1999). https://doi.org/10.1038/9142
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DOI: https://doi.org/10.1038/9142
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