Abstract
Treating rats with kainic acid induces status epilepticus (SE) and leads to the development of behavioral deficits and spontaneous recurrent seizures later in life. However, in a subset of rats, kainic acid treatment does not induce overt behaviorally obvious acute SE. The goal of this study was to compare the neuroanatomical and behavioral changes induced by kainate in rats that developed convulsive SE to those who did not. Adult male Wistar rats were treated with kainic acid and tested behaviorally 5 months later. Rats that had experienced convulsive SE showed impaired performance on the spatial water maze and passive avoidance tasks, and on the context and tone retention tests following fear conditioning. In addition, they exhibited less anxiety-like behaviors than controls on the open-field and elevated plus-maze tests. Histologically, convulsive SE was associated with marked neuron loss in the hippocampal CA3 and CA1 fields, and in the dentate hilus. Rats that had not experienced convulsive SE after kainate treatment showed less severe, but significant impairments on the spatial water maze and passive avoidance tasks. These rats had fewer neurons than control rats in the dentate hilus, but not in the hippocampal CA3 and CA1 fields. Correlational analyses revealed significant relationships between spatial memory indices of rats and neuronal numbers in the dentate hilus and CA3 pyramidal field. These results show that a part of the animals that do not display intense behavioral seizures (convulsive SE) immediately after an epileptogenic treatment, later in life, they may still have noticeable structural and functional changes in the brain.
Highlights
Temporal lobe epilepsy (TLE) can be associated with hippocampal cell loss and other structural changes in the medial temporal lobe region, such as fiber sprouting and synaptic reorganization [1,2,3]
From the 17 rats that had experienced convulsive status epilepticus (SE) 3 rats have died within 48 h following the treatment and 3 rats have died during the first month of the recovery period
One of the experimenters detected in these 2 rats repeated mouth and facial movements, but this observation was not confirmed by other experimenters
Summary
Temporal lobe epilepsy (TLE) can be associated with hippocampal cell loss (hippocampal sclerosis) and other structural changes in the medial temporal lobe region, such as fiber sprouting and synaptic reorganization [1,2,3]. Many studies have shown that the treatment of rats with kainic acid (KA), a specific agonist for glutamate receptors, induces acute status epilepticus (SE), accompanied by severe convulsive (motor) seizures, and that later in life these animals show spontaneous recurrent seizures, hippocampal cell loss and memory deficits [7,8,9] In this epilepsy model some rats are considerably more resistant to KA-induced convulsive SE than the others and, for that reason, are usually excluded from the studies [9,10,11,12,13]. Absolute numbers of neurons in the dentate gyrus hilus and pyramidal layers of the hippocampus proper were estimated using stereological approaches in order to compare the hippocampal cell loss between the two groups
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