One of the most frequent forms of epilepsy in humans is temporal lobe epilepsy. Characteristic to this form of the disease is the frequent pharmacoresistance and the association with behavioural disorders and cognitive impairment. The objective of our study was to establish the degree of cognitive impairment in a rat model of temporal lobe epilepsy after an initial epileptogenic exposure but before of the onset of the effect of long-duration epilepsy. Methods. For the experiment we used 11 rats. Status epilepticus was induced by systemic administration of a single dose of pilocarpine. The animals were continuously video-monitored to observe the occurrence of spontaneous recurrent seizures; during weeks 9-10 we performed eight-arm radial maze testing in order to assess the cognitive impairment. Results. Animals developed spontaneous recurrent seizures after a 14-21 day latency with a daily average seizure density of 0.79±0.43 during weeks 9-10. Epileptic rats had significantly more working memory errors per session, more reference memory errors and the number of visited arms was also significantly higher. Accuracy was also lower in the pilocarpine treated group. Interestingly significant differences disappeared after six days of trials. Conclusions. Our study shows behavioural deficits occurring after 9-10 weeks of epilepsy in the pilocarpine model of epilepsy applied to juvenile rats. In contrast to previous studies, we showed that juvenile rats with short duration of epilepsy are able to learn the behavioural task, therefore a morphopathological and/or behavioural "no-return point" regarding the development of severe cognitive impairment is not reached by status epilepticus alone.
Objective. Epilepsy is a neurological disorder that can be caused by many underlying pathologies. The epileptic and interictal manifestations that appear during the progression of chronic epilepsy are still not understood completely. One of the most frequent forms of this disease is temporal lobe epilepsy in which is clear involvement of the hippocampal formation. In order to study the electrografic progression of untreated seizures we used amygdala kindling in freely moving rats. Methods. Seven animals were implanted with bilateral hippocampal and prefrontal electrodes. A bipolar electrode, implanted in the lateral nuclei of the left amygdala was used for stimulation. The kindled group of animals was stimulated daily with the minimum current intensity needed to reach the afterdischarge threshold. Behavioral changes during kindling were scored according to the Racine scale. Results. The average seizure severity on the Racine scale was 2.6±0.4 by day 6 and 4.4±0.6 by day 20. The first spontaneous seizures appeared after 31 days of stimulation. During spontaneous seizures the preictal spike full width at half maximum increased gradually from 51±4msec to 110±5msec (p < 0.05) whereas the amplitude of the negative field potential deflection increased by 62% (p < 0.05). Conclusions. Our study showed that the progression of temporal lobe epilepsy, as seen in humans, can be reproduced in the kindling model with high fidelity. This study confirms in vivo the increase in preictal spike duration as well as the increase of the amplitude of negative field potential deflection during the preictal period.
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