The lesional and epileptogenic consequences of lithium–pilocarpine-induced status epilepticus are affected by previous exposure to isolated seizures: effects of amygdala kindling and maximal electroshocks
Section snippets
Animals
Male Wistar rats weighing 225–250 g, provided by Janvier Breeding Center (Le Genest-St-Isle, France), were housed under controlled standard conditions (light–dark cycle, lights on 7.00 a.m. to 7.00 p.m.), with food and water available ad libitum. All animal experimentation was performed in accordance with the rules of the European Committee Council Direction of 24 November 1986 (86/69/EEC) and the French Department of Agriculture (License No. 00733). For electrode implantation, all rats were
Rats subjected only to lithium–pilocarpine status epilepticus
In the sham-pilocarpine rats of both groups, the EEG and behavioral events leading to SE were similar to those described previously after the injection of a high dose of pilocarpine or lithium and pilocarpine.19., 23., 94.
Rats subjected to kindling and lithium–pilocarpine status epilepticus
The first electrographic spikes occurred after a mean duration of 27 min in both the sham-K-pilocarpine and the K-pilocarpine groups (Table 1). Rats developed stage 5 seizures at 7.8–7.9 min after the occurrence of the first electrographic seizures in both groups. All 18
Discussion
The exposure to amygdala kindling or repeated ECSs have different consequences on lesions and epilepsy induced by lithium–pilocarpine. Amygdala kindling decreases the sensitivity of rats to the convulsant, triggers large neuroprotective effects, mainly in the piriform and entorhinal cortices and in the hippocampus, but does not prevent epileptogenesis. Conversely, ECSs delay the onset of seizures, trigger more extended damage in the entorhinal and perirhinal cortices, and delay or prevent SRSs.
Conclusion
The present data show that repeated ECSs do not protect neurons from damage induced by lithium–pilocarpine SE, but prevent or delay the occurrence of SRSs. This apparent antiepileptic effect of ECS may relate to the extensive damage recorded in the entorhinal and perirhinal cortices that may inhibit the expression of motor seizures by preventing their propagation from the hippocampus. Conversely, amygdala kindling that triggers extensive neuroprotection in the limbic system but not the hilus
Acknowledgements
This work was supported by a grant from INSERM U398, and by a joint grant from the French League against Epilepsy and Cassenne-Marion Laboratories attributed to Véronique André.
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