Acetylcholinesterase as a potential target of acute neurotoxic effects of lindane in rats.

The aim of our study was to investigate the possible involvement of acetylcholinesterase (AchE) in mediating the early phase of acute lindane neurotoxicity in rats. Male Wistar rats (n = 48) were divided into following groups: 1. control, saline-treated group; 2. dimethylsulfoxidetreated group; 3. group that received lindane dissolved in dimethylsulfoxide, in a dose of 8 mg/kg intraperitoneally. Eight animals from each group were sacrificed 0.5 and 4 h after treatment and brain samples were prepared for further analysis. AchE activity (mitochondrial and synaptosomal fraction) was determined in cerebral cortex, thalamus, hippocampus and nc. caudatus spectrophotometrically. A significant increase in mitochondrial AchE activity was detected in cortex and nc. caudatus of lindane-treated animals 0.5 h after administration (p < 0.05). This rise was sustained in nc. caudatus within 4 h after treatment (p < 0.05). In contrast, activity of synaptosomal AchE fraction was significantly increased only in thalamus 4 h after lindane administration (p < 0.05). An increase in AchE activity may be involved in mediating acute neurotoxic effects of lindane, at least in some brain structures in rats.

High dose of ethanol decreases total spectral power density in seizures induced by D,L-homocysteine thiolactone in adult rats.

The effects of ethanol on epilepsy are very complex. Ethanol can have depressant as well as excitatory effect on different animal models of epilepsy. Systemic administration of homocysteine can trigger seizures. The aim of the present study was to examine the changes of total spectral power density after ethanol alone and together with homocysteine thiolactone in adult rats. Adult male Wistar rats were divided into following groups: 1. saline-injected, (control) C; 2. D, L-homocysteine thiolactone, H (8 mmol/kg); 3. ethanol, E (E(0.5), 0.5 g/kg; E(1), 1 g/kg; E(2), 2 g/kg) and 4. E (E(0.5), E(1), and E(2)) 30 min prior to H, EH (E(0.5)H, E(1)H and E(2)H). For EEG recordings three gold-plated screws were implanted into the skull. Our results demonstrate that ethanol, when applied alone, increased total EEG spectral power density of adult rats with a marked spectrum shift toward low frequency waves. In EH groups, increasing doses of ethanol exhibited a dose-dependent effect upon spectral power density. Ethanol increased EEG spectral power density in E(0.5)H and E(1)H group, comparing to the H group (p > 0.05), the maximal increase was recorded with the lowest ethanol dose applied. The highest dose of ethanol (E(2)H) significantly decreased total power spectra density, comparing to the H group. We can conclude that high doses of ethanol depressed marked increase in EEG power spectrum induced by D,L-homocysteine thiolactone.