TRPV1 Activation in Primary Cortical Neurons Induces Calcium-Dependent Programmed Cell Death.
TRPV1 Activation in Primary Cortical Neurons Induces Calcium-Dependent Programmed Cell Death.
复制标题
DOI：
10.5607/en.2013.22.1.51
复制
发表时间：
2013-03
影响因子：
2.4
通讯作者：
Lee JE
中科院分区：
文献类型：
--
作者：
Song J;Lee JH;Lee SH;Park KA;Lee WT;Lee JE
瞬时受体电位阳离子通道，亚家族V，成员1（TRPV 1，也称为香草素受体1）是一种检测辣椒素（辣椒的辛辣成分）和有毒热量的受体。尽管TRPV 1在初级伤害感受器中作为疼痛受体的功能已经得到了很好的证实，但它是否在大脑中表达仍存在争议。在这项研究中，原代皮层神经元的反应进行了研究。在这里，我们报告1）辣椒素诱导caspase-3依赖性程序性细胞死亡，这与一氧化氮和过氧亚硝酸盐的产生增加相一致; 2）长时间的辣椒素处理诱导caspase-3活化程度的稳定增加，这是通过去除辣椒素来防止的; 3）阻断钙进入和钙介导的信号传导可以防止辣椒素诱导的细胞死亡。这些结果表明皮质神经元表达TRPV 1，其长期激活会导致细胞死亡。
Transient receptor potential cation channel, subfamily V, member 1 (TRPV1, also known as vanilloid receptor 1) is a receptor that detects capsaicin, a pungent component of chili peppers, and noxious heat. Although its function in the primary nociceptor as a pain receptor is well established, whether TRPV1 is expressed in the brain is still under debate. In this study, the responses of primary cortical neurons were investigated. Here, we report that 1) capsaicin induces caspase-3-dependent programmed cell death, which coincides with increased production of nitric oxide and peroxynitrite ; that 2) the prolonged capsaicin treatment induces a steady increase in the degree of capase-3 activation, which is prevented by the removal of capsaicin; 3) and that blocking calcium entry and calcium-mediated signaling prevents capsaicin-induced cell death. These results indicate that cortical neurons express TRPV1 whose prolonged activation causes cell death.