期刊
JOURNAL OF PHYSIOLOGY-LONDON
卷 559, 期 1, 页码 35-40出版社
WILEY
DOI: 10.1113/jphysiol.2004.070763
关键词
-
Glycine is known to modulate immune cell responses. However, the physiological mechanisms underlying inhibitory effects of glycine on macrophages are not well understood. Here we show that glycine is capable of inducing inward currents in brain macrophages (microglia). In contrast to glycine, the glycine receptor agonist taurine failed to elicit currents. Glycine-evoked currents of brain macrophages were unaffected by strychnine, Cl--free extracellular solution, N-[3-(4'-fluorophenyl)-3-(4'-phenylphenoxy)propyl])sarcosine (NFPS) and amoxapine, but were abolished upon omission of extracellular Na+. Furthermore, glycine caused increases in the intracellular Na+ concentration and pronounced membrane depolarization. Glycine-evoked depolarization was Na+ dependent and occurred independently of the intracellular Cl- concentration. Similarly to glycine, glutamine and alpha-(methylamino)isobutyric acid (MeAIB) elicited inward currents in brain macrophages. In the presence of either glutamine or MeAIB, glycine-induced currents were inhibited. It is concluded that neither functional glycine receptors nor glycine transporters are expressed in brain macrophages. We suggest that glycine mediates its effects by activation of system A Na+-coupled neutral amino acid transporters.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据