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Homocysteine, endogenous sulphur – containing amino acid, displays neuroexcitatory effects and acts as a convulsant agent by still unclear mechanisms. Reported results on the role of nitric oxide (NO) in epileptogenesis are highly contradictory. NO levels could be decreased by N-nitro-L-arginine methyl ester (L-NAME), an inhibitor of enzyme NO synthase (NOS). The aim of the current study was to examine the effects of L-NAME on seizure susceptibility induced by subconvulsive dose of D,L homocysteine – thiolactone (HCT) in rats. Adult male Wistar albino rats were intraperitoneally (i.p.) treated with HCT 5.5 mmol/kg and observed for seizure behavioral manifestations during next 90 min. Increasing doses of L-NAME (200, 500 and 700 mg/kg, i.p., n=6, 7 and 8, respectively) or saline (n=9) were injected 30 min prior to HCT administration. Seizure episode severity was assessed using descriptive rating scale with four grades. L-NAME in doses of 500 and 700 mg/kg signifi cantly increased severity of homocysteine seizures (P<0.05) when compared with saline –injected rats. The lowest applied dose of L-NAME (200 mg/kg) had no statistically signifi cant effect on severity of seizures induced by HCT. Based on these results it cold be concluded that L-NAME, NOS inhibitor, potentiates convulsive properties of HCT.
This study examines the effects of ethanol on lindane-induced seizures in rats. The animals were divided into following groups: 1. saline, 2. DMSO (dimethylsulfoxide), 3. lindane dissolved in DMSO in the dose of 4, 6 or 8 mg/kg (L4, L6 and L8 groups, respectively), 4. ethanol 2 g/kg administered 30 min prior to lindane (protected groups AL4, AL6 and AL8) and 5. ethanol alone (2 g/kg). In order to determine ethanol concentration in plasma, blood samples were collected by cardiac puncture 30 and 60 min after ethanol injection. For EEG and power spectra recordings, electrodes were implanted into the skull. The lindane treatment resulted in a dose-dependent increase of seizure incidence and severity. The rats displayed severe seizure patterns characterized by high voltage spike-wave complexes, poly-spikes and sleep-like patterns in EEG, while the power spectra were intensively elevated in comparison to the corresponding controls. Ethanol alone led to increased EEG power spectra, which became dominant in the range of 0-4 Hz. For evaluation of anticonvulsant ethanol action we compared latency to seizure, incidence and seizure severity (scale from 0 to 4) in the examined groups. Ethanol diminished seizure incidence in AL4 and AL6 groups, decreased intensity of convulsions, and prolonged duration of latency period in AL8 group. We observed suppression of the EEG signs of lindane-provoked epileptiform activity in AL4 and AL6, but not in AL8 group. These results suggest that ethanol acted protectively on lindane-induced seizures and suppressed behavioral and epileptic EEG spiking activity.
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