Tian Shun-Lian, Jiang Hui, Zeng Yan, Li Ling-Li, Shi Jing
Department of Neurobiology and Key Laboratory of Neurological Disease of Hubei Province, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan 430030, PR China.
Neurosci Lett. 2007 May 29;419(2):93-8. doi: 10.1016/j.neulet.2007.04.020. Epub 2007 Apr 13.
Transient receptor potential melastatin 7 (TRPM7) channels are widely expressed in the nervous system; however, their function and regulation are largely unknown. This study aimed to explore whether the current mediated by TRPM7-like channels in rat CA1 hippocampal neurons could be modulated by nerve growth factor (NGF). Using whole-cell patch clamp techniques, we identified an outward-rectifying TRPM7-like current in hippocampal neurons freshly isolated from postnatal (10-day-old) rats. The outward component of this current was reversibly reduced by NGF in dose- and time-dependent manners, and this effect was substantially blocked by K252a, an inhibitor of TrkA. In addition, NGF-induced reduction of the TRPM7-like current was abolished by U73122, a phopholipase C inhibitor. In light of the abundance of NGF in hippocampus that express both TrkA and TRPM7, these results suggest that the function of TRPM7-like channels in hippocampal neurons may be regulated by NGF.
瞬时受体电位褪黑素7(TRPM7)通道在神经系统中广泛表达;然而,它们的功能和调节机制在很大程度上尚不清楚。本研究旨在探讨大鼠CA1海马神经元中由TRPM7样通道介导的电流是否可被神经生长因子(NGF)调节。运用全细胞膜片钳技术,我们在新生(10日龄)大鼠新鲜分离的海马神经元中鉴定出一种外向整流的TRPM7样电流。该电流的外向成分被NGF以剂量和时间依赖性方式可逆性降低,且这种效应被TrkA抑制剂K252a显著阻断。此外,磷脂酶C抑制剂U73122消除了NGF诱导的TRPM7样电流降低。鉴于海马体中同时表达TrkA和TRPM7的NGF含量丰富,这些结果表明海马神经元中TRPM7样通道的功能可能受NGF调节。