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Objectives To study the effects of the standardized extract from the leaves of Erythrina velutina in behavioural and oxidative parameters in the ketamine‐induced schizophrenia model. Methods Mice received ketamine (KET) or saline for 7 days. From 8th to 14th day, the animals received Erythrine (Eryt) (100, 200 or 400 mg/kg) or olanzapine (Olanz), 1 h after KET administration. At 14th day, 30 min after the last administration of KET, the open‐field and pre‐pulse inhibition (PPI) tests were performed. Then, the animals were sacrificed and the prefrontal cortex (PFC), hippocampus (HC) and striatum (ST) were dissected for the oxidative tests. Key findings Ketamine increased spontaneous locomotor activity and grooming. KET decreased the PPI, which was reversed by combining it with Eryt or olanzapine. KET decreased GSH concentration in PFC and ST this was reversed by Eryt. KET increased MDA concentration in PFC and HC this was reversed by Eryt. Eryt and Olanzapine reduced MDA concentration in ST when compared to KET group. Nitrite concentration was reduced by administration of KET in the PFC. Conclusions These results demonstrate that the standardized extract of E. velutina can prevent behavioural symptoms and oxidative stress induced by repeated doses of KET.

Background Schizophrenia is a chronic mental disorder, characterized by positive, negative and cognitive symptoms. In general, several plants have shown activity in diseases related to the central nervous system (e.g., Erythrina velutina (EEEV), also known as “mulungu”). For this reason, we aimed to investigate the effects of standardized ethanol extract obtained from the stem bark of EEEV on the schizophrenia-like behaviors induced by ketamine (KET) administration. Methods Swiss mice were treated with KET (20 mg/kg, i.p.) or saline for 14 days. In addition, from 8th to 14th days, saline, EEEV (200 or 400 mg/kg, p.o.) or olanzapine (OLAN 2 mg/kg, p.o.) were associated to the protocol. On the 14th day of treatment, schizophrenia-like symptoms were evaluated by the prepulse inhibition of the startle reflex (PPI), locomotor activity evaluated by the open field test (OFT), spatial recognition memory evaluated by the Y-maze task and social interaction test (SIT). Results KET has caused deficits in PPI, and it has also has caused hyperlocomotion in OFT and deficits in SIT as compared to control. EEEV in both doses used, reversed behavioral changes induced by KET, likewise results obtained with the administration of OLAN. Conclusions Taken together, the results demonstrate that the standard extract of EEEV was able to revert schizophrenia-like symptoms, due to the administration in repeated doses of ketamine. Thus, our findings lead to a new perspective for the use of EEEV an interesting alternative for drug discovery in schizophrenia.

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