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.