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去极化诱导的脑组织中[125I]脑源性神经营养因子的释放。

The depolarisation-induced release of [125I]BDNF from brain tissue.

作者信息

Androutsellis-Theotokis A, McCormack W J, Bradford H F, Stern G M, Pliego-Rivero F B

机构信息

Imperial College of Science, Technology and Medicine, Department of Biochemistry, London, UK.

出版信息

Brain Res. 1996 Dec 16;743(1-2):40-8. doi: 10.1016/s0006-8993(96)00981-x.

Abstract

The pattern of release of radioactive brain-derived neurotrophic factor ([125I]BDNF) from brain tissue was studied. Rat brain slices from cerebral cortex and synaptosomes from cerebral cortex and hippocampus were preloaded with [125I]BDNF. Depolarising stimulation by veratridine (final conc. 50 microM) and high KCl (final conc. 45 mM) caused a short-term, greatly enhanced depolarisation-induced release of [125I]BDNF during superfusion and batch protocol experiments. The results suggested that the evoked release was independent of the presence of extracellular calcium ions, but dependent on intracellular calcium ion stores, since the intracellular calcium ion chelator BAPTA-AM, but not the extracellular chelator EGTA abolished the high-potassium-induced [125I]BDNF release from synaptosomes. The release was blocked by tetrodotoxin (1 microM) when synaptosomes were stimulated by veratridine or potassium chloride. Short time-fraction (30 s) superfusion experiments showed that the [125I]BDNF release from synaptosomes appeared in two temporal phases.

摘要

研究了脑组织中放射性脑源性神经营养因子([125I]BDNF)的释放模式。用[125I]BDNF预加载来自大脑皮层的大鼠脑片以及来自大脑皮层和海马体的突触体。在灌注和批量实验中,藜芦碱(终浓度50微摩尔)和高钾(终浓度45毫摩尔)引起的去极化刺激导致[125I]BDNF的短期、去极化诱导释放显著增强。结果表明,诱发释放与细胞外钙离子的存在无关,但依赖于细胞内钙离子储存,因为细胞内钙离子螯合剂BAPTA-AM而非细胞外螯合剂EGTA消除了高钾诱导的突触体中[125I]BDNF的释放。当用藜芦碱或氯化钾刺激突触体时,释放被河豚毒素(1微摩尔)阻断。短时间片段(30秒)灌注实验表明,突触体中[125I]BDNF的释放在两个时间阶段出现。

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