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The present study was designed to investigate the influence of acute ethanol intake and its withdrawal on the anticonvulsant effect of alpha-tocopherol in penicillin-induced epileptiform activity. Ethanol-treated rats received a daily dose of 3 g/kg or 9.0 g/kg of 30% ethanol solution for 3 days. Thirty minutes after penicillin injection (500 units, i.c.), the most effective dose of alpha-tocopherol (500 mg/kg) was administered intramuscularly (i.m.). Acute administration of ethanol, in a dose of 3 g/kg, did not change either frequency or amplitude of penicillin-induced epileptiform activity, while dose of 9 g/kg ethanol significantly decreased the mean frequency of penicillin-induced epileptiform ECoG activity in the ethanol-treated group. Ethanol (9 g/kg) withdrawal also caused an increase in the amplitude of epileptiform ECoG activity in the withdrawal group. The results suggest that acute administration of high dose ethanol (9 g/kg) and alpha-tocopherol have some limited anticonvulsive effects in penicillin-induced epileptiform activity in rats.
Previous experimental studies have shown that various anesthetics alter the effects of cannabinoid agonists and antagonists on the cardiac response to different stimuli. Since no data have shown an interaction between urethane and cannabinoid signaling in epilepsy, we examined the suitability of urethane with regard to testing the effects of a cannabinoid CB1 receptor agonist and an antagonist on penicillin‑induced epileptiform activity in rats. Permanent screw electrodes for electrocorticographic (ECoG) recordings, and a permanent cannula for administration of the substances to the brain ventricles were placed into the cranium of rats. Epileptiform activity was induced by injection of penicillin through the cannula in conscious animal. The CB1 receptor agonist arachidonyl‑2‑chloroethylamide (ACEA; 7.5 μg) and the CB1 receptor antagonist [N‑(piperidin‑1‑yl)‑5‑(4‑iodophenyl)‑1‑(2,4‑dichlorophenyl)‑4‑methyl‑1H‑pyrazole‑3 carboxamide] (AM‑251; 0.25 μg) were administered intracerebroventricularly 30 minutes after the penicillin application in urethane‑anesthetized and conscious animals. Urethane completely eliminated spontaneous ictal events in ECoG recordings and reduced the frequency and total amount of epileptiform activity. It did not alter either the proconvulsant effects of AM‑251 or the anticonvulsant effects of ACEA on penicillin‑induced epileptiform activity. The electrophysiological evidence suggests that there is no possible interaction between urethane and cannabinoid CB1 receptors in this experimental model of epilepsy.
The aim of the present study is to understand the basic relationship between swimming exercise and natural course of epilepsy in animals by performing an electrophysiological study. For this purpose, male Wistar rats were submitted to daily swimming exercise program of three different durations. Animals were swim-exercised for 90 days with either 15 minutes, 30 minutes or 60 minutes/day. Thereafter, the epileptiform activity was induced by a single microinjection of penicillin (500 units) into the left somatomotor cortex. Short-duration swimming exercise (15 min per day for 90 days) decreased the mean frequency and amplitude of penicillin-induced epileptiform activity in the 70 and 90 minutes after penicillin injection compared to penicillin administered group, respectively. Moderate-duration (30 min per day for 90 days) and long-duration (60 min per day for 90 days) swimming exercise did not alter either the frequency or amplitude of epileptiform activity. The results of the present study provide electrophysiologic evidence that short-duration swimming exercise partially inhibits penicillin-induced epileptiform activity. These data also suggest that moderate and long-duration swimming exercise do not increase either the frequency or severity of seizure in the model of penicillin-induced epilepsy.
The benefits of regular exercise on brain health are undeniable. Long-term exercise increases the production of reactive oxygen species in brain. Therefore, athletes often consume antioxidant supplements to remedy exercise-related damage and fatigue during exercise. The aim of this study is to evaluate the role of ascorbic acid in the effects of different intensities of swimming exercise on the brain susceptibility to experimental epilepsy in rats. Ascorbic acid was administered intraperitoneally (ip) during three different swimming exercise programme for 90 days (15 min, 30 min, 90 min/day). The anticonvulsant activity regarding the frequency of epileptiform activity appeared in the 80 min after 500 units intracortical penicillin injection in 30 min and 90 min/day exercise groups. The administration of ascorbic acid (100 mg/kg, ip) did not alter the anticonvulsant properties seen in the in short-duration (15 min/day) swimming exercise group. The amplitude of epileptiform activity also became significant in the 110 and 120 min after penicillin injection in the moderate (30 min/day) and long duration (60 min/day) groups, respectively. The results of the present study provide electrophysiologic evidence that long-term administration of ascorbic acid causes anticonvulsant activities in the moderate and long-duration swimming exercise. Antioxidant supplementation such as ascorbic acid might be suggested for moderate and long-duration swimming exercise in epilepsy.
Regular exercise and amino acid supplementation, popular approaches toward the reduction of epileptic seizures, have been extensively researched. This study was conducted to evaluate the effects of treadmill exercise and L-tyrosine treatment on the frequency and amplitude of epileptiform activity in rats. A total of 32 male albino Wistar rats were randomly divided into four groups: control, exercise, L-tyrosine, and exercise + L-tyrosine. L-tyrosine was supplemented by oral gavage (500 mg/kg/day, 2.5 mL solution). The treatments were performed 5 days a week for 10 weeks. The rats were anesthetized and then administered 500 IU penicillin into the left cerebral cortex using a microinjector and electrocorticogram (ECoG) activity was recorded for 3 hours using a Power Lab data acquisition system. The frequency and the amplitude of the ECoG recordings were analyzed offline. Compared to the control group, spike frequency decreased significantly in all other groups. There was no statistically significant difference between the groups in terms of spike amplitude and latency. In this study, the effects of regularly administered treadmill exercise and L-tyrosine use on epileptiform activity were examined and evaluated together for the first time. The results of this study showed that regular exercise and L-tyrosine use decreased epileptiform activity. Further research and clinical trials are needed to investigate the extent to which L-tyrosine and physical activity interfere with the epileptic state by investigating different doses of L-tyrosine and different severity/ time/type of exercise protocols.
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