Section of the corpus callosum in kainic acid induced seizures in rats: behavioral, electroencephalographic and neuropathological study

E Hirsch,O.C Snead,I Gomez,T.Z Baram,M Vergnes

doi:10.1016/0920-1211(92)90096-c

Abstract

Clinical and experimental data suggest that the role of corpus callosum in epilepsy includes synchronization, spread, excitation and inhibition. Section of the corpus callosum (SCC) is known to be a useful therapy in selected types of generalized epilepsy i.e., tonic, atonic and generalized convulsive seizures, but not partial seizures which may be exacerbated by this procedure. The goal of this study was to determine the effect of SCC in the kainic acid (KA) model of limbic seizures in rats. Using several doses of KA (2.5, 5 and 10 mg/kg) injected systemically, we found a potentiation of the behavioral, electrographic and histological effects of KA in the SCC group of animals compared to the sham-operated control rats. A low dose of kainic acid (2.5 and 5 mg/kg) induced status epilepticus in the SCC animals, but not in the sham-operated control rats. These data demonstrate that in the KA model of temporal lobe seizures, SCC not only fails to protect, but actually intensifies seizures. This finding is compatible with the hypothesis that there is an inhibitory influence, via the corpus callosum, of the non epileptic neocortex on its contralateral homologue in the kainic acid model.

Highlights

Kainic acid (KA) is a rigid glutamate analogue, which induces electroencephalographic (EEG) and behavioral seizures in rats2*14.The behavioral and EEG aspects of the seizures are dose-dependent and progress over time to status epileptiCUS*~~~*B~e~h.avioral, EEG, metabolic, and neuropathological studies show that systemic KA preferentially activates seizures in the limbic system, Correspondence to: O.C
The goal of this study was to determine the effect of corpus callosum sectioning in the kainic acid model of focal limbic seizures and status epilepticus in rats
No ventral forebrain lesions were found. These data demonstrate no protective effect of complete Section of the corpus callosum (SCC) against seizures and status epilepticus in the kainic acid model

Summary

Introduction

Kainic acid (KA) is a rigid glutamate analogue, which induces electroencephalographic (EEG) and behavioral seizures in rats2*14.The behavioral and EEG aspects of the seizures are dose-dependent and progress over time to status epileptiCUS*~~~*B~e~h.avioral, EEG, metabolic, and neuropathological studies show that systemic KA preferentially activates seizures in the limbic system, Correspondence to: O.C. The corpus callosum serves primarily to connect the neocortex” of the two hemispheres, while the ventral hippocampal commissure connects the hip pocampus of each sidez. The role of the corpus callosum in epilepsy has been documented in a number of animal models of generalized or focal seizures in the cat, monkey and rat[3]. Erickson* showed that the corpus callosum is a substrate for propagation, bilateralization and generalization of partial seizures. The corpus callosum has been found to be necessary for bilateral synchronization of epileptic discharges in the feline generalized penicillin epilepsy modelm, pentylenetetrazol induced seizures in rats’s and in the genetic model of absence in rats3*

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