Abstract
Temporal lobe epilepsy (TLE) is a common neurological disease and antiseizure medication is often inadequate for preventing apoptotic cell death. Aerobic swimming exercise (EX) augments neurogenesis in rats when initiated immediately in the postictal period. This study tests the hypothesis that aerobic exercise also augments neurogenesis over the long term. Male Wistar rats (age of 4 months) were subjected to chemical lesioning using KA and to an EX intervention consisting of a 30 d period of daily swimming for 15 min, in one experiment immediately after KA lesioning (immediate exposure) and in a second experiment after a 60 d period of normal activity (delayed exposure). Morphometric counting of neuron numbers (NN) and dendritic branch points and intersections (DDBPI) was performed in the CA1, CA3, and dentate regions of hippocampus, in basolateral nucleus of amygdala, and in several areas of motor cortex. EX increased NN and DDBPI in the normal control and the KA-lesioned rats in all four limbic and motor cortex areas studied, after both immediate and 60 d delayed exposures to exercise. These findings suggest that, after temporal lobe epileptic seizures in rats, swimming exercise may improve neural plasticity in areas of the brain involved with emotional regulation and motor coordination, even if the exercise treatment is delayed.
Highlights
Temporal lobe epilepsy is associated with oxidative stress and apoptotic cell death in brain tissues and is often resistant to treatment with antiepileptic drugs, and progression of the disease produces adverse neurobehavioral sequelae [1, 2]
Temporal lobe epileptic seizures may spread to the amygdala where apnea is shown to occur by virtue of connectivity between amygdala and brainstem respiratory network nuclei [5]
These data demonstrate that the swimming exercise produced significant μm (a) increases in the numbers of surviving neurons in these areas of the brain, both in the presence and in the absence of kainic acid (KA) lesioning
Summary
Temporal lobe epilepsy is associated with oxidative stress and apoptotic cell death in brain tissues and is often resistant to treatment with antiepileptic drugs, and progression of the disease produces adverse neurobehavioral sequelae [1, 2]. Temporal lobe epileptic seizures may spread to the amygdala where apnea is shown to occur by virtue of connectivity between amygdala and brainstem respiratory network nuclei [5]. Neurogenesis in the amygdala has not been extensively studied in that regard. Connectivity between these limbic areas and motor cortex is less direct and not very robust, likely relayed through the cingulate and insular cortices [7]. Motor deficits in temporal lobe epilepsy are uncommonly reported and the effects of kainateinduced seizures on motor cortex have not been systematically studied. Aerobic exercise is a treatment for inhibiting neuronal apoptosis associated with aging and maintaining
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