Epileptic Model Induced By FeCL₃ And The Effects Of Melatonin On Epilepsy

Epilepsy is a common neurologic disease and does harm to people hardly. However, the mechanism of epilepsy is not definited. The common character of epilepsy is recurrent transient paroxysms of hyperactive brain function. Epileptic discharge is the result of neuron depolarization shift. And lipid peroxidation induced by free radical reaction can infect on Na+ -, Ca2+ influx , making neuronal membrane depolarization .In recent years, an increasing amount of data has been published involving melatonin (MT) in the control of brain function. There are three major mechanisms: (1) Scavenging free radicals and suppressing peroxidation. (2) depressing CNS excitability, a.increasing the inhibitory neurotransmitter activity (mainly acting on GABA-benzodiazepine receptor complex), b. decreasing the excitatory neurotransmitter activity (acting on excitatory aminoacids). c. changing membrane permeability and subsequently membrane potential and /or a second messenger system. ( 3 )effecting on others hormone, such as insuline. From these mechanisms, we can infer that MT has anticonvulsant effect. The study set up an epileptic model induced by FeCL3 and observed the effect of MT on the epileptic rat's EEG recording and behavior in awake. In addition, we determinated the effect of MT on the concentration of malondialdehyde (MDA) and activity of superoxide dismutase (SOD) in epileptic rat's brain tissue. Method1. Effect of melatonin on behavior and EEG in rats with epilepsy induced by FeCL3Thirty-two male Sprague-Dawley rats, weighing 250-300g, were used in experiment. Each group was eight. The experimental groups were conducted as follow : 1 Control group. (g)0,03mmol/kg MT group. (3)0.1 mmol/kg MT group.?0.3mmol/kg MT group.According to Kabuto, four epidural stainless steel screw electrodes were placed in the calvarium 2.5mm anterior to and 6mm behind the coronal sutures, and 2 and 3mm from the sagittal suture. In the central of occipital bone was communal electrode. To allow intracerebral administration of FeCL3, a burr hole was established over the region of the sensorrimotor cortex, 1mm posterior and 1mm lateral to the bregma. To record EEG, the electrodes were attached to a polygraph record (1 left frontal 梠ccipital bone(F3 ?A)2 right frontal ?occipital bone(F4桝).3 left parietal梠ccipital bone (C3?A), ﹔ight parietal ?occipital bone(C4 ?A)). A week later, melatonin (0.03, 0.1, or 0.3mmol/kg in 5% ethanol solution ) or vehicle (5% ethanol, as control)was injected i.p. Five min after melatonin injection, SOCnmol FeCL3 was injected.2.Determination of the concentration of MDAThirty-two male Sprague-Dawley rats, weighing 250-300g, were used in experiment. Each group was eight. The experimental groups were conducted as follow: ㎞ormal control.2 Physiologic saline group.3 FeCL3 group.4 0.3mmol/kg MT+ FeCL3group.Injection site was same as the described above. The brain was dissected carefully and removed after 60 min. Tissue samples were measured 3x3mm and contained the injection site. The samples were then washed with ice-cold saline and weighed. In the next step, the samples were homogenized in 9 times physiologic saline. Finally, The homogenates were centrifuged at 6000r/min. The concentration of MDA was detected using method of thiobarbituricacid in 721 spectrometer. 3.Determination of activity of SODDiluted the homogenates to 1% by physiologic saline. The activity of SOD was examined using xanthine oxidase method in 721 spectrometer. Result and discussionl.The epileptic model induced by FeCL3 is a stable model and all animals had typical epileptic behaviors and epileptic discharges. 2.0.1 mmol/kg and 0.3mmol/kg group of MT decreased the accumulated time of epileptic discharges and the times of >10 second epileptic discharges. The effect of 0.3mmol/kg group was better than O.lmmol/kg and 0.03mmol/kg group. 0.3mmol/kg group prolonged the latencies of epileptic discharge. In addition, MT reduced seizure degree.3.1ntracerebral administration of FeCL3 rose con...