We examined the influence of seizures and carbamazepine (CBZ) on spiking rates in kindled cats. In the first experiment, spiking rates were measured before and after seizures, with and without CBZ. CBZ was administered immediately after seizures in order not to affect them. Spiking rates were measured over 9 h during the different sleep stages. In a second experiment, CBZ was administered before and after seizures so as to affect seizure strength and thus measure its effect on spiking. Results confirmed earlier findings of a large increase in spiking following a stage 6 seizure in fully kindled animals. We also established that: (1) repeated daily seizures caused a further increase in spiking until a ceiling was reached; (2) increased spiking was not a direct effect of postictal alterations in sleep stages; (3) CBZ, despite its effectiveness as an anticonvulsant, did not reduce spiking but rather increased it; (4) postictal increases in spiking were related to seizure 'strength'. These findings support the hypothesis that spiking rates are primarily influenced by seizure occurrence, as was found in patients with temporal lobe seizures, and that anticonvulsants act differently on seizures and spikes. This emphasizes the possibility of distinct pathophysiological mechanisms for interictal spikes and seizures.

Effects of seizures and carbamazepine on interictal spiking in amygdala kindled cats.

GIGLI, Gian Luigi;
1991-01-01

Abstract

We examined the influence of seizures and carbamazepine (CBZ) on spiking rates in kindled cats. In the first experiment, spiking rates were measured before and after seizures, with and without CBZ. CBZ was administered immediately after seizures in order not to affect them. Spiking rates were measured over 9 h during the different sleep stages. In a second experiment, CBZ was administered before and after seizures so as to affect seizure strength and thus measure its effect on spiking. Results confirmed earlier findings of a large increase in spiking following a stage 6 seizure in fully kindled animals. We also established that: (1) repeated daily seizures caused a further increase in spiking until a ceiling was reached; (2) increased spiking was not a direct effect of postictal alterations in sleep stages; (3) CBZ, despite its effectiveness as an anticonvulsant, did not reduce spiking but rather increased it; (4) postictal increases in spiking were related to seizure 'strength'. These findings support the hypothesis that spiking rates are primarily influenced by seizure occurrence, as was found in patients with temporal lobe seizures, and that anticonvulsants act differently on seizures and spikes. This emphasizes the possibility of distinct pathophysiological mechanisms for interictal spikes and seizures.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11390/856271
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