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多巴胺能系统激活对鲈鱼(Dicentrarchus labrax)摄食行为和生长性能的影响:一种自投喂方法。

Effects of dopaminergic system activation on feeding behavior and growth performance of the sea bass (Dicentrarchus labrax): a self-feeding approach.

机构信息

Department of Fish Physiology and Biotechnology, Instituto de Acuicultura de Torre de la Sal, Consejo Superior de Investigaciones Científicas (IATS-CSIC), Castellón, Spain.

出版信息

Horm Behav. 2013 Jun;64(1):113-21. doi: 10.1016/j.yhbeh.2013.05.008. Epub 2013 Jun 6.

Abstract

Dopamine is synthesized from l-dopa and subsequently processed into norepinephrine and epinephrine. Any excess neurotransmitter can be taken up again by the neurons to be broken down enzymatically into DOPAC. The effect of dopamine on mammalian food intake is controversial. Mice unable to synthesize central dopamine die of starvation. However, studies have also shown that central injection of dopamine inhibits food intake. The effect of dopaminergic system in the fish feeding behavior has been scarcely explored. We report that the inclusion of l-dopa in the diets results in the activation of sea bass central dopaminergic system but also in the significant increase of the hypothalamic serotonin levels. Dietary l-dopa induces a decrease of food intake and feed conversion efficiency that drives a decline of all growth parameters tested. No behavioral effects were observed after l-dopa treatment. l-dopa treatment stimulated central expression of NPY and CRF. It suggests that CRF might mediate l-dopa effects on food intake but also that CRF neurons lie downstream of NPY neurons in the hierarchical forebrain system, thus controlling energy balance. Unexpectedly, dietary administration of haloperidol, a D2-receptor antagonist, cannot block dopamine effects but also induces a decline of the food intake. This decrease seems to be a side effect of haloperidol treatment since fish exhibited a decreased locomotor activity. We conclude that oral l-dopa inhibits sea bass food intake and growth. Mechanism could also involve an increase of hypothalamic serotoninergic tone.

摘要

多巴胺由左旋多巴合成,随后被加工成去甲肾上腺素和肾上腺素。任何多余的神经递质都可以被神经元再次摄取,并通过酶促反应分解为 DOPAC。多巴胺对哺乳动物摄食的影响存在争议。不能合成中枢多巴胺的小鼠会死于饥饿。然而,研究也表明,中枢注射多巴胺会抑制摄食。多巴胺能系统在鱼类摄食行为中的作用尚未得到充分探索。我们报告称,在饮食中添加左旋多巴会激活鲈鱼中枢多巴胺能系统,但也会显著增加下丘脑 5-羟色胺水平。饮食中的左旋多巴会导致摄食量和饲料转化率下降,从而导致所有测试的生长参数下降。左旋多巴处理后没有观察到行为效应。左旋多巴处理刺激了 NPY 和 CRF 的中枢表达。这表明 CRF 可能介导了左旋多巴对摄食的影响,但也表明 CRF 神经元位于 NPY 神经元下游的脑前层级系统中,从而控制能量平衡。出乎意料的是,膳食中给予多巴胺 D2 受体拮抗剂氟哌啶醇不能阻断多巴胺的作用,反而会导致摄食量下降。这种下降似乎是氟哌啶醇治疗的副作用,因为鱼的运动活性降低。我们得出结论,口服左旋多巴抑制鲈鱼的摄食和生长。其机制可能还涉及下丘脑 5-羟色胺能活动的增加。

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