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Deficit of quantal release of GABA in experimental models of temporal lobe epilepsy

Nature Neuroscience volume 2, pages 499–500 (1999)Cite this article

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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Figure 1: Deficit of GABAergic miniature activity in epileptic animals.
Figure 2: Perisomatic GABAergic terminals in control and epileptic animals.

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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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Authors and Affiliations

  1. INSERM U29, 123 Bld de Port Royal, Paris, 75014, France

    J.C. Hirsch, C. Agassandian, Y. Ben-Ari, M. Esclapez & C. Bernard

  2. Universidad Europea de Madrid, Dpt. Ciencias Morfológicas y Fisiología, Madrid, 28670, Spain

    A. Merchán-Pérez

  3. Instituto Cajal, CSIC, Madrid, 28002, Spain

    A. Merchán-Pérez & J. DeFelipe

Authors
  1. J.C. Hirsch
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  2. C. Agassandian
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  3. A. Merchán-Pérez
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  4. Y. Ben-Ari
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  5. J. DeFelipe
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  6. M. Esclapez
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  7. C. Bernard
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Correspondence to C. Bernard.

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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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