Sánchez Olea R, Pasantes-Morales H
Institute of Cellular Physiology, National University of Mexico, Mexico City.
Neurochem Res. 1990 May;15(5):535-40. doi: 10.1007/BF00966213.
Exposure of a crude synaptosomal fraction to K+ concentrations ranging from 25 to 100 mM evokes the release of [3H]taurine and [3H]GABA. These high concentrations of K+ induce, besides depolarization, a marked synaptosomal swelling, which is prevented by replacing chloride in the solutions with the largely impermeant anion gluconate. The depolarizing effect of K+ is unaffected by omission of chloride. The K(+)-evoked release of taurine seems related to K(+)-induced changes in synaptosomal volume rather than to a depolarizing effect, since it is totally calcium-independent but is abolished by reducing chloride and by making solutions hypertonic with mannitol. The release of [3H]GABA, in contrast is unaffected in chloride-free or hypertonic solutions.
将粗制突触体组分暴露于浓度范围为25至100 mM的K⁺中，会引发[³H]牛磺酸和[³H]γ-氨基丁酸（GABA）的释放。除了去极化作用外，这些高浓度的K⁺还会引起明显的突触体肿胀，而用基本上不能透过的阴离子葡萄糖酸盐替代溶液中的氯离子可防止这种肿胀。K⁺的去极化作用不受氯离子缺失的影响。K⁺诱发的牛磺酸释放似乎与K⁺诱导的突触体体积变化有关，而不是与去极化作用有关，因为它完全不依赖于钙，但通过减少氯离子和用甘露醇使溶液变为高渗状态可使其释放被消除。相比之下，[³H]GABA的释放在无氯或高渗溶液中不受影响。
