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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Taurine-mediated aggression is abolished via 5-HT1A antagonism and serotonin depletion in zebrafish
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Taurine-mediated aggression is abolished via 5-HT1A antagonism and serotonin depletion in zebrafish

机译：牛磺酸介导的侵略通过5-ht1a拮抗作用和Zebrafish中的血清素枯萎废除

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Taurine is one of the most abundant amino acids in vertebrates involved in important physiological functions, including osmoregulation, membrane stability, and neuronal activity. The pleiotropic effects of taurine support the existence of different mechanisms of action (e.g., modulation of GABA(A), strychnine-sensitive glycine, and NMDA receptors), which can play a role in aggressive-related responses. However, the mechanisms underlying the effects of taurine on aggression are still poorly understood. Because aggression has been associated with diverse central mechanisms, especially serotonergic activity, we aimed to investigate the involvement of this system in taurine-induced aggression in zebrafish. We treated adult zebrafish with rho-chlorophenylalanine (rho CPA), an inhibitor of the semtonin synthesis, as well as 5-HT1A receptor antagonist and agonist (WAY100135 and buspirone, respectively). Taurine effects were tested individually at three concentrations (42, 150, and 400 mg/L) for 60 min. We further analyzed the effects on aggression and locomotion using the mirror-induced aggression test. Taurine concentration that changed behavioral responses was selected to the succeeding pharmacological experiments using rho CPA, WAY100135, and buspirone. We found that buspirone did not alter the aggression. Yet, 42 mg/L taurine increased aggression, which was abolished by rho CPA and WAY100135, indicating the involvement of 5-HT1A receptors in taurine-mediated aggression. These set of data support an indirect mechanism mediating taurine-induced aggression via serotonin release and activation of 5-HT1A receptors in zebrafish. While the exact mechanisms underlying aggression are still unclear, our novel findings reveal a key role of the serotonergic system in the effects of taurine, supporting the use of zebrafish models to understand the neural basis of aggression in vertebrates.
机译：牛磺酸是脊椎动物体内含量最丰富的氨基酸之一，参与重要的生理功能，包括渗透调节、膜稳定性和神经元活动。牛磺酸的多效性效应支持存在不同的作用机制（例如，GABA（A）、士的宁敏感甘氨酸和NMDA受体的调节），这些机制可在攻击性相关反应中发挥作用。然而，牛磺酸对攻击性影响的机制仍知之甚少。由于攻击性与多种中枢机制有关，尤其是5-羟色胺能活动，我们旨在研究该系统在牛磺酸诱导的斑马鱼攻击中的作用。我们用rho-氯苯基丙氨酸（rho-CPA）以及5-HT1A受体拮抗剂和激动剂（分别为WAY100135和丁螺环酮）治疗成年斑马鱼，rho-CPA是一种半胱氨酸合成抑制剂。在三种浓度（42、150和400 mg/L）下分别测试60分钟的牛磺酸效应。我们使用镜像诱导攻击试验进一步分析了对攻击和运动的影响。通过使用rho-CPA、WAY100135和丁螺环酮进行后续药理学实验，选择改变行为反应的牛磺酸浓度。我们发现丁螺环酮并没有改变攻击性。然而，42 mg/L牛磺酸增加了攻击性，rho-CPA和WAY100135消除了这一点，表明5-HT1A受体参与了牛磺酸介导的攻击性。这些数据支持一种间接机制，通过5-HT1A受体在斑马鱼体内的5-HT1A释放和激活，介导牛磺酸诱导的攻击。虽然攻击性的确切机制尚不清楚，但我们的新发现揭示了5-羟色胺能系统在牛磺酸作用中的关键作用，支持使用斑马鱼模型来理解脊椎动物攻击性的神经基础。

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