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首页> 外文期刊>Journal of psychopharmacology >Regulation of adenosine A(2A) receptor gene expression in a model of binge eating in the amygdaloid complex of female rats
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Regulation of adenosine A(2A) receptor gene expression in a model of binge eating in the amygdaloid complex of female rats

机译：雌性大鼠杏仁骨络合物中泪味术模型中腺苷A（2A）受体基因表达的调节

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Background: Pharmacological treatment approaches for eating disorders, such as binge eating disorder and bulimia nervosa, are currently limited. Methods and aims: Using a well-characterized animal model of binge eating, we investigated the epigenetic regulation of the A(2A) Adenosine Receptor (A(2A)AR) and dopaminergic D2 receptor (D2R) genes. Results: Gene expression analysis revealed a selective increase of both receptor mRNAs in the amygdaloid complex of stressed and restricted rats, which exhibited binge-like eating, when compared to non-stressed and non-restricted rats. Consistently, pyrosequencing analysis revealed a significant reduction of the percentage of DNA methylation but only at the A(2A)AR promoter region in rats showing binge-like behaviour compared to the control animals. Focusing thus on A(2A)AR agonist (VT 7) administration (which inhibited the episode of binge systemically at 0.1 mg/kg or intra-central amygdala (CeA) injection at 900 ng/side) induced a significant increase of A(2A)AR mRNA levels in restricted and stressed rats when compared to the control group. In addition, we observed a significant decrease in A(2A)AR mRNA levels in rats treated with the A(2A)AR antagonist (ANR 94) at 1 mg/kg. Consistent changes in the DNA methylation status of the A(2A)AR promoter were found in restricted and stressed rats after administration of VT 7 or ANR 94. Conclusion: We confirm the role of A(2A)AR in binge eating behaviours, and we underline the importance of epigenetic regulation of the A(2A)AR gene, possibly due to a compensatory mechanism to counteract the effect of binge eating. We suggest that A(2A)AR activation, inducing receptor gene up-regulation, could be relevant to reduction of food consumption.
机译：背景：目前有限的饮食疾病的药理治疗方法，如狂犬病患者和贪食症。方法和宗旨：使用良好表征的狂犬病动物模型，研究了A（2a）腺苷受体（A（2a）Ar）和多巴胺能D2受体（D2R）基因的表观遗传调节。结果：基因表达分析显示，与非应激和非限制性大鼠相比，乳腺碱复合物中的受体MRNA的受体MRNA的选择性增加。始终如一地，焦磷酸化分析显示DNA甲基化百分比的显着降低，但仅在与对照动物相比的大鼠中的A（2a）Ar启动子区的大鼠中。因此聚焦在（2A）AR激动剂（VT 7）给药（其在900ng /侧系统上系统性地抑制了0.1mg / kg或中央中央淋巴碱（CEA）注射）诱导了a（2a与对照组相比，受限制和压力大鼠的AR mRNA水平。此外，我们观察到用1mg / kg处理的大鼠（2a）Ar拮抗剂（ANR 94）处理的大鼠中的（2A）AR mRNA水平的显着降低。在施用VT 7或ANR 94后，在受限制和应激大鼠中发现A（2a）Ar启动子的DNA甲基化状态的一致变化。结论：我们确认了（2a）ar在狂暴吃行为中的作用，我们强调e（2A）AR基因的表观遗传调节，可能是由于补偿机制来抵消狂犬病的效果。我们建议诱导受体基因上调的（2A）AR激活，可能与减少食品消费。

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