levetiracetam and coriaria-lactone

To investigate the antiepileptic and protective effects of intravenous levetiracetam (iv LEV) in the rhesus monkey model of acute status epilepticus (SE).. Thirty minutes before intraperitoneal induction of SE by Coriaria lactone (CL), rhesus monkeys were treated with LEV (15 or 150 mg/kg) delivered intravenously as a single bolus. CL dose and epileptic behavior were recorded. Electroencephalography (EEG) was performed before and during the experiment. All rhesus monkeys were killed after 1-month video monitoring and processed for pathological investigation of neuronal injury, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining, and glial fibrillary acidic protein (GFAP) staining.. No animal exhibited spontaneous seizures during 1-month video monitoring. Development of acute SE was significantly inhibited in the group given 150 mg/kg LEV, compared with controls and the 15 mg/kg LEV group. Delayed latency, reduction of SE duration, decreased cumulative time of tonic convulsions, slight severity of SE, and a high CL induction dose were observed in the high LEV dose group (p<0.05). The EEG showed less frequent epileptic discharges in the group administered with 150 mg/kg LEV. Hematoxylin and eosin (H&E) staining, ultrastructural examination, TUNEL and GFAP staining revealed serious damage, including neuron loss, swollen mitochondrion, and strong positivity for TUNEL in the hippocampus and thalamus of controls, whereas moderate damage in the group administered with 15 mg/kg LEV, and very mild damage in the 150 mg/kg LEV group. Gliosis was found in the hippocampus of controls, not in the LEV groups and normal rhesus monkey.. The study supports the antiepileptic and protective effect of pretreatment with intravenous LEV in rhesus monkey model with SE.

Topics: Administration, Intravenous; Animals; Anticonvulsants; Disease Models, Animal; Humans; Lactones; Levetiracetam; Macaca mulatta; Male; Neurons; Piracetam; Status Epilepticus

To test the effect of Levetiracetam (LEV) on the sodium currents of rat hippocampal neurons exposed to epileptogenic coriaria lactone (CL).. Acutely isolated Sprague-Dawley Rat hippocampal neurons were subjected to the whole-cell mode of patch clamp under experimental conditions designed to detect voltage-gated sodium currents. The CL (0.2 mg/mL) was used to increase the sodium currents of the neurons. Then the LEV was added (150 or 300 micromol/L) to test the effect of LEV on the peak current amplitudes through a comparison with the control group in which extracellular solution was added instead and the group in which nothing was added. Another. group was pretreated with 300 micromol/L of LEV before the neutrons were treated with the CL.. The maximum peak amplitudes (MPA) of the sodium currents increased 36.92% +/- 2.84% by the 150 micromol/L of LEV (P < 0.05), similar to those exposed to the CL only (P > 0.05). The increase of MPA of the sodium currents by the 300 micromol/L of LEV (16.58% +/- 1.56%) was less than those exposed to the CL only (P < 0.05). However, no significant difference was found between the 300 micromol/L LEV treated group and the control group (P > 0.05). The MPA of the sodium currents of LEV pretreated neutrons increased 32.86% +/- 6.73% (P < 0.05), similar to those without pretreatment (P > 0.05).. The LEV does not decrease the sodium currents of rat hippocampal neurons induced by the CL. The antiepileptic action of LEV has nothing to do with the neuronal voltage-gated sodium channels.

Topics: Action Potentials; Animals; Anticonvulsants; Cells, Cultured; Hippocampus; Lactones; Levetiracetam; Neurons; Patch-Clamp Techniques; Piracetam; Rats; Rats, Sprague-Dawley; Sodium Channels