No abstract

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.

No abstract

Alcohol addiction is a chronic, relapsing and progressive brain disease with serious consequences for health. Compulsive use of alcohol is associated with the capacity to change brain structures involved with the reward pathway, such as ventral striatum. Recent evidence suggests a role of chromatin remodeling in the pathophysiology of alcohol dependence and addictive-like behaviors. In addition, neuroadaptive changes mediated by the brain-derived neurotrophic factor (BDNF) seems to be an interesting pharmacological target for alcoholism treatment. In the present study, we evaluated the effects of the deacetylase inhibitor valproic acid (VPA) (300mg/kg) on the conditioned rewarding effects of ethanol using conditioned place preference (CPP) (15% v/v; 2g/kg). Ethanol rewarding effect was investigated using a biased protocol of CPP. BDNF levels were measured in the ventral striatum. Ethanol administration induced CPP. VPA pretreatment did not reduce ethanol-CPP acquisition. VPA pretreatment increased BDNF levels when compared to ethanol induced-CPP. VPA pretreatment increased BDNF levels even in saline conditioned mice. Taken together, our results indicate a modulatory effect of VPA on the BDNF levels in the ventral striatum. Overall, this study brings initial insights into the involvement of neurotrophic mechanisms in the ventral striatum in ethanol-induced addictive-like behavior.