NOOTROPIC EFFECT OF NICOTINE ON CARBON-MONOXIDE (CO)-INDUCED DELAYED AMNESIA IN MICE

The effects of nicotine on carbon monoxide (CO)-induced amnesia in mic e were investigated using a step-down type passive avoidance task. Mic e were exposed to CO 3 times at 1-h intervals, 7 days before the first training and retention test and 24 h after the first training session . Memory deficiency occurred in mice when training commenced more than 3 days after CO exposure (delayed amnesia): the median step-down late ncy in the retention test of the CO-exposed group was significantly sh orter than that of the control group. Administration of (-)-nicotine ( 15.6 and 31.3 nmol/kg, IP) 15 min before the first training session pr olonged the step-down latency in the CO-exposed group, but (+)-nicotin e did not. To determine whether this effect of (-)nicotine was mediate d via nicotinic cholinergic receptors, we attempted to block its actio n using a nicotinic acetylcholine receptor antagonist (mecamylamine). Mecamylamine (1.25 mu mol/kg) blocked the effect of (-)-nicotine (31.3 nmol/kg) on delayed amnesia. Administration of (-)-nicotine (15.6-62. 5 nmol/kg) immediately after the first training session failed to amel iorate learning ability in the CO-exposed group. These results suggest that (-)-nicotine potentiates the nicotinic cholinergic neuronal syst em and may potentiate acquisition of memory.