Zoccarato F, Alexandre A
Department of Biological Chemistry, University of Padova, Italy.
Biochem Biophys Res Commun. 1996 Feb 6;219(1):198-204. doi: 10.1006/bbrc.1996.0205.
The treatment of cerebrocortical synaptosomes with low concentrations of H2O2 induces a long-lasting inhibition of the Ca2+ -dependent release of glutamate induced by KCl or ionomycin, without interfering with the cytosolic calcium and without damaging the synaptosomes (Zoccarato, F., Valente, M., and Alexandre, A. (1995) J. Neurochem. 64, 2552-2558). We report now that the inhibition exerted by H2O2 decreases (from 50 +/- 9% to 25 +/- 11%) if exocytosis is triggered by high (80 mM) rather than by low (30 mM) KCl. Similarly the inhibition decreases when glutamate release is triggered by high rather than by low ionomycin. The decreased inhibition by H2O2 on increasing KCl is accompanied by an increase of [Ca2+]i. We conclude that the treatment with H2O2 decreases the CA2+ sensitivity of the synaptosomal exocytotic apparatus.
用低浓度过氧化氢处理大脑皮质突触体可诱导对由氯化钾或离子霉素引起的谷氨酸钙依赖性释放产生持久抑制，且不干扰胞质钙，也不损伤突触体（佐卡拉托，F.，瓦伦特，M.，以及亚历山大，A.（1995年）《神经化学杂志》64卷，2552 - 2558页）。我们现在报告，如果胞吐作用由高浓度（80 mM）而非低浓度（30 mM）氯化钾触发，过氧化氢施加的抑制作用会降低（从50±9%降至25±11%）。同样，当谷氨酸释放由高浓度而非低浓度离子霉素触发时，抑制作用也会降低。随着氯化钾浓度增加，过氧化氢抑制作用的降低伴随着胞内钙浓度[Ca2+]i的增加。我们得出结论，用过氧化氢处理会降低突触体胞吐装置对钙离子的敏感性。
