Many evidences suggest a protective role of phenolic compounds on mood disorders. We aimed to assess the effect of the açaí seed extract (ASE) on anxiety induced by periodic maternal separation (PMS) in adult male rats. Animals were subdivided into six groups: Control, ASE, fluoxetine (FLU), PMS, PMS+ASE, and PMS+FLU. For PMS, pups were separated daily from the dam for 3hrs between postnatal day (PN)2–PN21. ASE (200mg/Kg/day) and FLU (10mg/Kg/day) were administered by gavage for 34 days after stress induction, starting at PN76. In PN106 and PN108, the rats were submitted to open field (OF) and forced swim tests, respectively. In PN110 the rats were sacrificed by decapitation. ASE increased the time spent in the center area in OF test, glucocorticoid receptors in the hypothalamus, TRKB receptors in the hippocampus, nitrite levels and antioxidant activity in brainstem from PMS+ASE group compared with the PMS group. ASE also reduced the corticotropin-releasing hormone plasma levels, norepinephrine adrenal levels, and oxidative damage in the brainstem from adult male offspring submitted to PMS. In conclusion, ASE treatment has an anti-anxiety effect in rats submitted to PMS by reducing hypothalamus-pituitary-adrenal axis reactivity and increasing NO-BDNF-TRKB pathway and antioxidant defense in the central nervous system. Novelty • Anti-anxiety and antioxidant effect of açaí in early life stress. • ASE reduces hypothalamus-pituitary-adrenal axis reactivity. • The anxiolytic effect of ASE may involve the activation of the NO-BDNF-TRKB pathway in the central nervous system.

The beneficial effects of drugs that act via nicotinic acetylcholine receptors (nAChRs) on Parkinson's disease (PD) symptomatology may explain the negative correlation between cigarette smoking and risk of this neurological condition. Varenicline, an α4β2 nAChR partial agonist approved for smoking cessation treatments, could be valuable for PD treatment. Here, we investigated varenicline effects in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) PD mouse model. From postnatal day (PN) 90 to PN119, male C57BL/6 mice were exposed daily to varenicline (2 mg/kg) by gavage. After that, MPTP was injected (30 mg/kg, ip ) once a day for five days. At PN125, locomotor and anxiety-like effects were assessed with the open field test. At PN126, immobile behavior was assessed with the forced swimming test. At PN127, the frontal cerebral cortex was collected to evaluate dopamine and DOPAC levels. To verify whether varenicline was protective during the MPTP insult, a separate group of MPTP animals received varenicline from PN90 to PN124. MPTP reduced cortical dopamine content and increased dopamine turnover. Those effects were not reversed by varenicline treatment. Interestingly, varenicline reversed the MPTP-induced hyperactivity in the open field. Both maintenance of varenicline treatment during MPTP exposure or its interruption before MPTP exposure elicited similar results. No alterations were observed in anxiety-like behavior or in immobility time. Altogether, these findings suggested that varenicline treatment reduced the MPTP-induced hyperactivity, but did not protect against dopaminergic damage. Based on this partial protective effect, varenicline could exert neuroprotective effects on circuits that control motor activity in PD.