Schizophrenia is one of the most disabling
mental disorders that affects up to 1 % of the population worldwide. Although the causes of this disorder remain unknown, it has been extensively characterized by a broad range of emotional, ideational and
cognitive impairments. Studies indicate that
schizophrenia affects
neurotransmitters such as
dopamine,
glutamate and
acetylcholine. Recent studies suggest that
rivastigmine (an
acetylcholinesterase inhibitor) is important to improve the
cognitive symptoms of
schizophrenia. Therefore, the present study evaluated the protective effect of
rivastigmine against the
ketamine-induced behavioral (hyperlocomotion and cognitive deficit) and biochemical (increase of
acetylcholinesterase activity) changes which characterize an animal model of
schizophrenia in rats. Our results indicated that
rivastigmine was effective to improve the cognitive deficit in different task (immediate memory, long term memory and short term memory) induced by
ketamine in rats. Moreover, we observed that rivastigmina reversed the increase of
acetylcholinesterase activity induced by
ketamine in the cerebral cortex, hippocampus and striatum. However,
rivastigmine was not able to prevent the
ketamine-induced hyperlocomotion. In conslusion, ours results indicate that
cholinergic system might be an important therapeutic target in the physiopathology of
schizophrenia, mainly in the cognition, but additional studies should be carried.