钡离子不支持大鼠大脑皮质突触体中的突触小泡回收。
Ba2+ does not support synaptic vesicle retrieval in rat cerebrocortical synaptosomes.
作者信息
Cousin M A, Robinson P J
机构信息
Children's Medical Research Institute, Wentworthville, NSW, Australia.
出版信息
Neurosci Lett. 1998 Aug 28;253(1):1-4. doi: 10.1016/s0304-3940(98)00610-7.
To investigate whether any specific requirement for extracellular Ca2+ exists in the control synaptic vesicle retrieval, we examined the ability of the divalent cation Ba2+ to substitute for Ca2+ in both vesicle exocytosis and endocytosis. Ba2+ stimulated glutamate release from rat cerebrocortical synaptosomes. Ba2+-evoked release was inhibited by bafilomycin A1, indicating release was via exocytosis of synaptic vesicles. However, Ba2+ did not stimulate vesicle retrieval, monitored by a FM2-10-based retrieval assay. Therefore synaptic vesicle retrieval in central nerve terminals has a specific requirement for extracellular Ca2+ and the Ca2+ receptor for retrieval has a different cation specificity to the Ca2+ receptor for exocytosis.
为了研究在突触小泡回收的调控过程中是否存在对细胞外Ca2+的特定需求，我们检测了二价阳离子Ba2+在小泡胞吐和内吞过程中替代Ca2+的能力。Ba2+刺激大鼠大脑皮质突触体释放谷氨酸。巴弗洛霉素A1抑制了Ba2+诱发的释放，表明该释放是通过突触小泡的胞吐作用实现的。然而，基于FM2-10的回收检测法监测结果显示，Ba2+并未刺激小泡回收。因此，中枢神经末梢的突触小泡回收对细胞外Ca2+有特定需求，且回收过程中的Ca2+受体与胞吐作用中的Ca2+受体具有不同的阳离子特异性。
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