Abstract
Administration of pilocarpine causes epilepsy in rats if status epilepticus (SE) is induced at an early age. To determine in detail the electrophysiological patterns of the epileptogenic activity in these animals, 46 Wistar rats, 7-17 days old, were subjected to SE induced by pilocarpine and electro-oscillograms from the cortex, hippocampus, amygdala, thalamus and hypothalamus, as well as head, rostrum and vibrissa, eye, ear and forelimb movements, were recorded 120 days later. Six control animals of the same age range did not show any signs of epilepsy. In all the rats subjected to SE, iterative spike-wave complexes (8.1 0.5 Hz in frequency, 18.9 9.1 s in duration) were recorded from the frontal cortex during absence fits. However, similar spike-wave discharges were always found also in the hippocampus and, less frequently, in the amygdala and in thalamic nuclei. Repetitive or single spikes were also detected in these same central structures. Clonic movements and single jerks were recorded from all the rats, either concomitantly with or independently of the spike-wave complexes and spikes. We conclude that rats made epileptic with pilocarpine develop absence seizures also occurring during paradoxical sleep, showing the characteristic spike-wave bursts in neocortical areas and also in the hippocampus. This is in contrast to the well-accepted statement that one of the main characteristics of absence-like fits in the rat is that spike-wave discharges are never recorded from the hippocampal fields.
Highlights
Epidemiological studies indicate that human epileptic disorders frequently have their onset early in life
The most significant findings of the present study are: i) permanent absence-like epilepsy develops in adult rats in which status epilepticus (SE) has been provoked by pilocarpine administration 7 to 17 days after birth; ii) iterative spike-wave discharges (SWD) occur bilaterally in the neocortex (8.1 ± 0.5 Hz in frequency, 18.9 ± 9.1 s in duration); iii)
During SWD the rats are generally immobilized, as in human absence seizures, but clonic movements and single jerks may occur concomitantly or dissociated from the SWD; iv) the neocortical SWD are similar to those found in all genetically epileptic rats; v) the SWD bursts can be entirely suppressed by ethosuximide; vi) similar SWD always occur in the hippocampus and frequently appear in the basolateral nucleus of the amygdala, thalamic ventrolateral nucleus and hypothalamic ventromedial nucleus; vii) SWD may occur during paradoxical sleep
Summary
Epidemiological studies indicate that human epileptic disorders frequently have their onset early in life. Mortality due to SE ranges from 2.5 to 20% in adults [5] and may reach moderately higher values of up to 25% in children [2,3,4,5,6,7,8] These data suggest that SE is a prominent factor in epilepsy, as demonstrated experimentally in rats and mice [9,10,11,12,13,14]. Late epileptic seizures may occur years after SE [4] and it should be pointed out that in children and adults who die of SE, lesions have been found in several areas of the brain [2,4,8]
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