Acute stress is an important factor in the development of anxiety disorders. Zebrafish are an organism model widely used by studies that aim to describe the events in the brain that control stress-elicited anxiety. the goal of the current study was to evaluate the pattern of cell activation in the telencephalon of adult zebrafish and the role of the GABAergic system on the modulation of anxiety-like behavior evoked by acute restraint stress. Zebrafish that underwent acute restraint stress presented decreased expression of the c-fos protein in their telencephalon as well as a significant decrease in GABA release. The data also supports that decreased GABA levels in zebrafish brains have diminished the activation of GABAA receptors eliciting anxiety-like behavior. Taken together these findings have helped clarify a neurochemical pathway controlling anxiety-like behavior evoked by acute stress in zebrafish while also opening the possibility of new perspective opportunities to use zebrafish as an animal model to test anxyolitic drugs that target the GABAergic system. open Scientific RepoRtS | (2020) 10:5551 | https://doi.
Anxiety is a common symptom associated with high caffeine intake. Although the neurochemical mechanisms of caffeine-induced anxiety remain unclear, there are some evidences suggesting participation of oxidative stress. Based on these evidences, the current study is aimed at evaluating the possible protective effect of alpha-tocopherol (TPH) against anxiety-like behavior induced by caffeine (CAF) in zebrafish. Adult animals were treated with CAF (100 mg/kg) or TPH (1 mg/kg)+CAF before behavioral and biochemical evaluations. Oxidative stress in the zebrafish brain was evaluated by a lipid peroxidation assay, and anxiety-like behavior was monitored using light/dark preference and novel tank diving test. Caffeine treatment evoked significant elevation of brain MDA levels in the zebrafish brain, and TPH treatment prevented this increase. Caffeine treatment also induced anxiety-like behavior, while this effect was not observed in the TPH+CAF group. Taken together, the current study suggests that TPH treatment is able to inhibit oxidative stress and anxiety-like behavior evoked by caffeine.
Background: Açaí (Euterpe oleracea) has a rich nutritional composition, showing nutraceutical and protective effects in several organs. In this study, the effects of an açaí-enriched diet on motor performance, anxiety-like behavior, and memory retention were deeply investigated.
Methods: Eight-week male Wistar rats were fed with an Euterpe oleracea (EO) pulp-enriched diet, an olive oil-enriched (OO) diet (polyunsaturated fatty acid [PUFA] fat control diet), or a chow diet for 31 days (28 days pre-treatment and 3 days during behavioral tests). Afterward, animals were submitted to a battery of behavioral tests to evaluate spontaneous motor behavior (open-field test), anxiety-like behavior (elevated plus maze and open-field test), and memory retention (step-down). Oxidative stress in the hippocampus was evaluated by a lipid peroxidation assay.
Results: EO-enriched diet did not influence the body weight and food intake but increased the glucose plasmatic level after 31 days under this diet. However, a similar fat-enriched diet stimulated a marked weight gain and reduced the food intake, followed by changes in the plasmatic lipid markers. EO-enriched diet preserved the motor spontaneous performance, increased the exploration in the aversive environment (anxiolytic-like effects), and elevated the latency to step-down (improved memory retention). The EO-enriched diet also reduced the level of lipid peroxidation in the hippocampus. These positive effects of EO-enriched diet can greatly support the usage of this diet as a preventive therapy.
Conclusion: Taken together, the current study suggests that Euterpe oleracea-enriched diet promotes anxiolytic-like effects and improves memory consolidation, possibly due to the reduced levels of lipid peroxidation in the hippocampus.
Anxiety disorder is a well-recognized condition observed in subjects submitted to acute stress. Although the brain mechanisms underlying this disorder remain unclear, the available evidence indicates that oxidative stress and GABAergic dysfunction mediate the generation of stress-induced anxiety. Cannabinoids are known to be efficient modulators of behavior, given that the activation of the cannabinoid receptors type-1 (CB1 receptors) induces anxiolytic-like effects in animal models. In the present study, we aimed to describe the effects of the stimulation of the CB1 receptors on anxiety-like behavior, oxidative stress, and the GABA content of the brains of zebrafish submitted to acute restraint stress (ARS). The animals submitted to the ARS protocol presented evident anxiety-like behavior with increased lipid peroxidation in the brain tissue. The evaluation of the levels of GABA in the zebrafish telencephalon presented decreased levels of GABA in the ARS group in comparison with the control. Treatment with ACEA, a specific CB1 receptor agonist, prevented ARS-induced anxiety-like behavior and oxidative stress in the zebrafish brain. ACEA treatment also prevented a decrease in GABA in the telencephalon of the animals submitted to the ARS protocol. Overall, these preclinical data strongly suggest that the CB1 receptors represent a potential target for the development of the treatment of anxiety disorders elicited by acute stress.
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