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 γ -aminobutyric acid (GABA)ergic inhibition in pyramidal neurons is still functional in temporal lobe epilepsy...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1997-10, Vol.94 (22), p.12151-12156
Main Authors: Esclapez, M, Hirsch, J C, Khazipov, R, Ben-Ari, Y, Bernard, C
Format: Article
Language:English
Subjects:
Action Potentials
Animal models
Animals
Arborization
Axons
Biological Sciences
Dendrites
Electric current
Epilepsy
Epilepsy, Temporal Lobe - chemically induced
GABA-A Receptor Antagonists
In Vitro Techniques
Interneurons
Interneurons - cytology
Interneurons - physiology
Male
Neural Inhibition - physiology
Neurobiology
Neurology
Neurons
Neuroscience
Patch-Clamp Techniques
Pyramidal cells
Pyramidal Cells - physiology
Rats
Rats, Wistar
Receptors, GABA - metabolism
Rodents
Seizures
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Summary: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 γ -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.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.94.22.12151