Operative GABAergic inhibition in hippocampal CA1 pyramidal neurons in experimental epilepsy.
Patch-clamp recordings of CA1 interneurons and pyramidal cells were performed in hippocampal slices from kainate- or pilocarpine-treated rat models of temporal lobe epilepsy. We report that gamma-aminobutyric acid (GABA)ergic inhibition in pyramidal neurons is still functional in temporal lobe epilepsy because: (i) the frequency of spontaneous GABAergic currents is similar to that of control and (ii) focal electrical stimulation of interneurons evokes a hyperpolarization that prevents the generation of action potentials. In paired recordings of interneurons and pyramidal cells, synchronous interictal activities were recorded. Furthermore, large network-driven GABAergic inhibitory postsynaptic currents were present in pyramidal cells during interictal discharges. The duration of these interictal discharges was increased by the GABA type A antagonist bicuculline. We conclude that GABAergic inhibition is still present and functional in these experimental models and that the principal defect of inhibition does not lie in a complete disconnection of GABAergic interneurons from their glutamatergic inputs.[1]References
- Operative GABAergic inhibition in hippocampal CA1 pyramidal neurons in experimental epilepsy. Esclapez, M., Hirsch, J.C., Khazipov, R., Ben-Ari, Y., Bernard, C. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
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