Background: Supplementation of omega-3 fatty acids has shown efficacy to prevent conversion to schizophrenia in ultra-high risk population. In this study we evaluated the efficacy of omega-3 in preventing ketamine-induced effects in an animal model of schizophrenia and its effect on BDNF serum levels. Methods: Forty-eight Wistar male rats were included. Twenty-four received 0.8g/kg omega-3 and 24 tween, both groups at the 30Th day of life for 15 days. Each group was split in two 12-animals groups to receive along the following 7 days 25 mg/kg of ketamine or saline intra-peritoneal. The total treatment period was 22 days. Locomotor and exploratory activity (open-field task), memory test (inhibitory avoidance test) and social interaction between pairs (latency time to first contact, number and time of contacts) were evaluated at the 52nd day of life. Bloods for BDNF were withdrawal at the 53rd day of life. Results: Social interactions were decreased in time and number of contacts, and latency time to first contact was increased in ketamine group. Ketamine increased covered distances in 5, 10 and 15 minutes. Ketamine+omega-3 were not different than controls and omega-3 alone in 10 and 15 minutes. On the inhibitory avoidance memory test, omega-3 has prevented ketamine-induced impairment on working, short and late memories. BDNF levels were higher in ketamine+omega-3 group (p=0.009). Conclusions: Omega-3, in a ketamine-induced model of schizophrenia, prevents in adolescents Wistar male rats the equivalent in humans of positive, negative and, cognitive symptoms of schizophrenia. Moreover it increases BDNF in prevention treatment of ketamine effects.

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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.

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