[The effects of some cholinergic drugs on cognitive processes and oxidative stress in rat]

Reactive oxygen species (ROS) are produced within the body during oxygen metabolism and living organisms have developed several defense mechanisms to protect themselves from oxidative stress. Under normal conditions, ROS and antioxidant systems are in balance. Oxidative stress is caused by the imbalance between production of pro-oxidants and the antioxidant defenses. The defense mechanisms include antioxidant enzymes like superoxide dismutase (SOD) or glutathione peroxidase (GPX) and several no enzymatic free radical scavengers. It has been proposed that the progressive increase in ROS and consequent oxidative damage play the major role in neurodegenerative disorders. Learning and memory show an age-related decline and this age-associated impairment extends to spatial memory tasks. Furthermore, the neural circuits between the prefrontal cortex and striatum are also involved in spatial memory. In our previous studies, we have shown the facilitatory role of nicotine and cholinergic system in learning and memory processes. In the present study, we examined whether oxidative stress contributes to the memory deficits induced by muscarinic acetylcholine receptors (mAchRS) blocked by scopolamine. We also examined the effect of nicotine on oxidative stress, and also if nicotine could attenuated the learning and memory deficits induced by blocked of mAchRS. We observed that the levels of SOD and GPX decrease in rats mAchRS blockade by scopolamine (0.75 mg/kg body weight i.p.), and the level of malondialdehyde (MDA) increase in same rats, compared with saline-treated rats. Therefore, our results suggest that the oxidative stress contributes to the learning and memory deficits in rats.