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首页> 外文期刊>The European Journal of Neuroscience >Enhanced food intake after stimulation of hypothalamic P2Y1 receptors in rats: modulation of feeding behaviour by extracellular nucleotides.
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Enhanced food intake after stimulation of hypothalamic P2Y1 receptors in rats: modulation of feeding behaviour by extracellular nucleotides.

机译：刺激大鼠下丘脑P2Y1受体后食物摄取增加：通过细胞外核苷酸调节进食行为。

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The present study was aimed to clarify the role of purinergic signalling in the regulation of ingestion behaviour. The ATP/ADP analogues 2-methylthioATP (2-MeSATP) and adenosine 5'-O-(2-thiodiphosphate) (ADPbetaS) increased the food intake after intracerebroventricular infusion in 18-h food-deprived rats. This effect was abolished by pretreatment with the non-selective P2X/P2Y receptor antagonist pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS) or the selective P2Y1 receptor antagonist MRS 2179, respectively. The stimulation of food intake mediated by ADPbetaS was also blocked by pretreatment with the nitric oxide synthase (NOS) inhibitor Nw-nitro-L-arginine methylester (L-NAME), as well as with the inhibitor of the soluble guanylyl cyclase 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), suggesting that the orexigenic effect seems to be closely related with the ensuing formation of nitric oxide. The immunohistochemical staining indicating a co-localization of P2Y1 receptor- and nNOS-immunoreactivities in a population of neurons in the ventromedial hypothalamic nucleus (VMH) agrees with this assumption. Further experiments with the direct local application of these compounds into the VMH and lateral hypothalamic nucleus (LH) show that the stimulation of P2Y1 receptors in these functionally antagonistic brain regions exerts an increased food intake. Hence, different signal transduction mechanisms may operate in the VMH and LH. Our assumption is supported by distinct effects of the NOS inhibitor L-NAME in these two hypothalamic nuclei. The present data suggest that ATP/ADP, acting as extracellular signal molecules in the rat brain, are involved in the regulation of food intake, possibly depending on P2Y1-receptor-mediated nitric oxide production.
机译：本研究旨在阐明嘌呤能信号在调节饮食行为中的作用。 ATP / ADP的类似物2-甲基硫代ATP（2-MeSATP）和腺苷5'-O-（2-硫代二磷酸）（ADPbetaS）增加了脑室内输注18小时食物匮乏大鼠的食物摄入量。通过分别使用非选择性P2X / P2Y受体拮抗剂吡ido醛磷酸盐-6-偶氮苯基-2'，4'-二磺酸（PPADS）或选择性P2Y1受体拮抗剂MRS 2179进行预处理，可以消除这种作用。用一氧化氮合酶（NOS）抑制剂Nw-硝基-L-精氨酸甲酯（L-NAME）以及可溶性鸟苷酰环化酶1H- []预处理也可以阻止ADPbetaS介导的食物摄取刺激。 1,2,4]恶二唑并[4,3-a]喹喔啉-1-酮（ODQ），表明致癌作用似乎与随后形成的一氧化氮密切相关。免疫组化染色表明在下丘脑下丘脑核（VMH）的神经元群体中P2Y1受体和nNOS免疫反应性共定位，这与该假设一致。将这些化合物直接局部应用到VMH和下丘脑外侧核（LH）中的进一步实验表明，在这些功能拮抗的大脑区域刺激P2Y1受体会增加食物摄入量。因此，不同的信号转导机制可以在VMH和LH中运行。我们的假设得到了NOS抑制剂L-NAME在这两个下丘脑核中不同作用的支持。目前的数据表明，ATP / ADP作为大鼠脑中的细胞外信号分子，参与了食物摄入的调节，可能取决于P2Y1受体介导的一氧化氮的产生。

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