Motor map expansion in the pilocarpine model of temporal lobe epilepsy is dependent on seizure severity and rat strain |
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Authors: | Nicole A. Young Jennifer Vuong Lana J. Ozen Corey Flynn G. Campbell Teskey |
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Affiliation: | aDepartment of Psychology, University of Calgary, Calgary, Alberta, Canada, T2N 1N4;bDepartment of Cell Biology and Anatomy, University of Calgary, 3330 Hospital Drive N.W., Calgary, Alberta, Canada, T2N 4N1 |
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Abstract: | Functional alterations in movement representations (motor maps) have been observed in some people with epilepsy and, under experimental control, electrically-kindled seizures in rats also result in persistently larger motor maps. To determine if a single event of status epilepticus and its latent consequences can affect motor map expression, we assessed forelimb motor maps in rats using the pilocarpine model of temporal lobe epilepsy. We examined both pilocarpine-induced seizures, and status epilepticus (SE) in two strains that differ in their propensity for epileptogenesis; Wistar and Long-Evans. Pilocarpine was administered intraperitoneally at dosages that resulted in equivalent proportions of seizures, SE, and survival in both strains. Rats from both strains were given saline injections as a control. Diazepam was administered to all rats to attenuate seizure activity and promote survival. All rats had high-resolution movement representations derived using standard intracortical microstimulation methodologies at 48 h, 1 week, or 3 weeks following treatment. Pilocarpine-induced seizures only gave rise to motor map enlargement in Wistar rats, which also showed interictal spiking, and only at 3 weeks post-treatment indicating altered motor map expression in this strain following a latent or maturational period. Pilocarpine-induced SE yielded larger motor maps at all time points in Wistar rats but only a transient (48 h) map expansion in Long-Evans rats. Our results demonstrate that seizures and SE induced by a convulsant agent alter the functional expression of motor maps that is dependent on seizure severity and a genetic (strain) predisposition to develop epileptiform events. |
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Keywords: | Epilepsy Intracortical microstimulation Pilocarpine Map expansion Neuroplasticity Seizure Status epilepticus Kindling |
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