导读： 常永生课题组于2017年01月在”Cell Reports” 杂志发表研究论文“Trpc5 mediates acute leptin and serotonin effects via Pomc neurons”。此研究发现瞬时受体电位5（TrpC5）离子通道在调节前阿片黑素细胞皮质激素（POMC）神经细胞活性，控制机体能量平衡和血糖稳态以及介导瘦素和五羟色胺信号通路过程中的重要作用。 

链接：http://www.sciencedirect.com/science/article/pii/S2211124716317946?via%3Dihub。 

图：

        下丘脑POMC 神经细胞上LepR(瘦素受体)和Ht2Cr（五羟色胺受体）可激活POMC神经细胞，影响食欲和机体产热等生理过程。POMC 神经元细胞活性增加，需要细胞去极化，该过程需要离子通道参与，但是确切的离子通道不清楚。中国医学科学院基础医学研究所，“医学分子生物学国家重点实验室”的常永生研究团队通过研究发现瞬时受体电位5（TrpC5）离子通道在调节前阿片黑素细胞皮质激素（POMC）神经细胞活性，控制机体能量平衡和血糖稳态以及介导瘦素和五羟色胺信号通路过程中的重要作用。 

        【摘要】： The molecular mechanisms underlying acute leptin and serotonin 2C receptor-induced hypophagia remain unclear. Here, we show that neuronal and pro-opiomelanocortin (Pomc)-specific loss of transient receptor potential cation 5 (TrpC5) subunits is sufficient to decrease energy expenditure and increase food intake resulting in elevated body weight. Deficiency of Trpc5 subunits in Pomc neurons is also sufficient to block the anorexigenic effects of leptin and serotonin 2C receptor (Ht2Cr) agonists. The loss of acute anorexigenic effects of these receptors is concomitant with a blunted electrophysiological response to both leptin and Ht2Cr agonists in arcuate Pomc neurons. We also demonstrate that the Ht2Cr agonist lorcaserin-induced improvements in glucose and insulin tolerance are blocked by TrpC5 deficiency in Pomc neurons. Together, our results link TrpC5 subunits in the brain with leptin- and serotonin 2C receptor-dependent changes in neuronal activity, as well as energy balance, feeding behavior, and glucose metabolism. 

        本文通讯作者为常永生研究员，第一作者高永博士。该研究工作得到了国家自然科学基金的支持。 

医学分子生物学国家重点实验室