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花生四烯酸乙醇胺和三氯蔗糖改变奖励系统中的 ΔFosB 表达。

Anandamide and sucralose change ΔFosB expression in the reward system.

机构信息

Faculty of Sciences, Toluca, State of Mexico, Mexico.

Toluca, State of Mexico, Mexico, Faculty of Veterinary Medicine and Zootechnics, Autonomous University of the State of México.

出版信息

Neuroreport. 2020 Feb 5;31(3):240-244. doi: 10.1097/WNR.0000000000001400.

DOI:10.1097/WNR.0000000000001400
PMID:31923023
Abstract

Food reward has been studied with highly palatable stimuli that come from natural additives such as sucrose. The most common food additive is sucralose, a noncaloric sweetener present in many food products of daily intake. The role of anandamide [N-arachidonylethanolamide (AEA)], an endogenous cannabinoid, has been widely studied in food behavior. Studies have shown that cannabinoids, such as AEA, 2-Arachidonilglycerol, and Tetrahydrocannabinol, can provoke hyperphagia, because they enhance the preference and intake of sweet and high-fat food. Taste perception is mediated by receptors taste type 1 receptor 3 (T1R3); therefore, there could be a synergistic effect between receptors CB1 and T1R3. This could explain why cannabinoids could change sweet taste perception and therefore the activity of neural nuclei involved in taste and reward. In this study, we evaluated the activity of dopaminergic nuclei implicated in food reward after the chronic administration of AEA (0.5 mg/kg bw) and sucralose intake (0.02%). We analyzed the expression of ΔFosB by immunohistochemistry. Our results show that the chronic administration of AEA and sucralose intake induces an overexpression of ΔFosB in the infralimbic cortex (Cx), nucleus accumbens (NAc) core, shell, and central nucleus of amygdala (Amy). These results suggest that the possible interaction between receptors CB1 and T1R3 has consequences not only in taste perception but also that AEA intervenes in the activity of dopaminergic nuclei such as the NAc, and that the chronic administration AEA and sucralose intake induce long-term changes in the reward system.

摘要

食物奖赏已经通过研究来自天然添加剂(如蔗糖)的高可口刺激物进行了研究。最常见的食品添加剂是三氯蔗糖,它是一种非营养性甜味剂,存在于许多日常摄入的食品中。内源性大麻素[N-花生四烯酰乙醇胺(AEA)]的作用在食物行为中得到了广泛研究。研究表明,大麻素,如 AEA、2-花生四烯酰甘油和四氢大麻酚,可以引起暴食,因为它们增强了对甜和高脂肪食物的偏好和摄入。味觉感知是由味觉受体 1 型受体 3(T1R3)介导的;因此,CB1 和 T1R3 受体之间可能存在协同作用。这可以解释为什么大麻素可以改变甜味感知,从而改变与味觉和奖赏相关的神经核团的活动。在这项研究中,我们评估了慢性给予 AEA(0.5mg/kg bw)和三氯蔗糖摄入(0.02%)后与食物奖赏相关的多巴胺能核团的活性。我们通过免疫组织化学分析了 ΔFosB 的表达。我们的结果表明,慢性给予 AEA 和三氯蔗糖摄入会导致扣带回下皮质(Cx)、伏隔核(NAc)核心、壳和杏仁中央核(Amy)中 ΔFosB 的过度表达。这些结果表明,CB1 和 T1R3 受体之间的可能相互作用不仅会影响味觉感知,而且 AEA 还会干预 NAc 等多巴胺能核团的活动,慢性给予 AEA 和三氯蔗糖摄入会导致奖赏系统的长期变化。

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