Newly formed excitatory pathways provide a substrate for hyperexcitability in experimental temporal lobe epilepsy

Temporal lobe epilepsy (TLE) in humans and animals is associated with axonal sprouting of glutamatergic neurons and neosynaptogenesis in the hippocampal formation. We examined whether this plasticity of excitatory pathways contributes to an increased level of glutamatergic excitation in the CA1 regi...

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Bibliographic Details
Published in:Journal of comparative neurology (1911) 1999-06, Vol.408 (4), p.449-460
Main Authors: Esclapez, Monique, Hirsch, June C., Ben-Ari, Yezekiel, Bernard, Christophe
Format: Article
Language:English
Subjects:
Animals
Axons - physiology
CA1
Dendrites - physiology
Electrophysiology
Epilepsy, Temporal Lobe - pathology
Epilepsy, Temporal Lobe - physiopathology
Glutamic Acid - physiology
hippocampus
Hippocampus - pathology
Hippocampus - physiopathology
Image Processing, Computer-Assisted
kainate
Lysine - analogs & derivatives
Male
Nerve Net - physiopathology
Neural Pathways - pathology
Neural Pathways - physiopathology
Neuronal Plasticity - physiology
Neurons - physiology
pilocarpine
plasticity
Pyramidal Cells - physiology
rat
Rats
Rats, Wistar
Seizures - chemically induced
Seizures - physiopathology
Synapses - physiology
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Summary:Temporal lobe epilepsy (TLE) in humans and animals is associated with axonal sprouting of glutamatergic neurons and neosynaptogenesis in the hippocampal formation. We examined whether this plasticity of excitatory pathways contributes to an increased level of glutamatergic excitation in the CA1 region of rats experiencing chronic spontaneous limbic seizures following kainic acid or pilocarpine treatment. In chronic cases, we report an extensive axonal sprouting of CA1 pyramidal neurons, with many axonal branches entering the pyramidal cell layer and stratum radiatum, regions that are not innervated by axonal collaterals of CA1 pyramidal neurons in control animals. Concurrently with this anatomical reorganization, a large increase of the spontaneous glutamatergic drive is observed in the dendrites and somata of CA1 pyramidal cells. Furthermore, electrical activation of the reorganized CA1 associational pathway evokes epileptiform bursts in CA1 pyramidal cells. These findings suggest that reactive plasticity could contribute to the hyperexcitability of CA1 pyramidal neurons and to the propagation of seizures in these two models of TLE. J. Comp. Neurol. 408:449–460, 1999. © 1999 Wiley‐Liss, Inc.
ISSN:0021-9967
1096-9861
DOI:10.1002/(SICI)1096-9861(19990614)408:4<449::AID-CNE1>3.0.CO;2-R