IPF, a vesicular uptake inhibitory protein factor, can reduce the Ca(2+)-dependent, evoked release of glutamate, GABA and serotonin.
IPF, a vesicular uptake inhibitory protein factor, can reduce the Ca(2+)-dependent, evoked release of glutamate, GABA and serotonin.
复制标题
IPF 是一种囊泡摄取抑制蛋白因子，可以减少 Ca(2) 依赖性诱发的谷氨酸、GABA 和血清素的释放。
DOI：
10.1046/j.1471-4159.2001.00120.x
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发表时间：
2001
影响因子：
4.7
通讯作者：
Ueda,T
中科院分区：
文献类型：
--
作者：
Tamura,Y;Ozkan,ED;Bole,DG;Ueda,T
神经末梢的突触小泡在神经传递中起着关键作用。神经递质积累到突触囊泡中是由不同的囊泡转运蛋白催化的，利用 V 型质子泵 ATP 酶产生的电化学质子梯度。然而，人们对递质池大小的调节知之甚少，特别是在氨基酸神经递质方面。我们之前提供了证据，证明存在一种有效的内源性抑制蛋白因子 (IPF)，它会导致分离纯化的突触小泡中谷氨酸和 GABA 的积累减少。在这项研究中，我们证明 IPF 最集中在突触体胞质部分，当引入突触体时，它会导致谷氨酸的钙依赖性胞吐（但不是钙独立）释放以浓度依赖性方式减少。相比之下，α-胞质蛋白（非红系血影蛋白）在结构上与 IPF 相关并被认为是 IPF 的前体，但缺乏这种抑制活性。突触内 IPF 还导致 GABA 和单胺神经递质血清素的胞吐释放减少。 IPF 是否影响体内多种神经递质的囊泡储存取决于 IPF 的定位。这些结果提出了 IPF 可能通过充当一种或多种神经递质的量子大小调节剂来调节突触传递的可能性。
Synaptic vesicles in the nerve terminal play a pivotal role in neurotransmission. Neurotransmitter accumulation into synaptic vesicles is catalyzed by distinct vesicular transporters, harnessing an electrochemical proton gradient generated by V‐type proton‐pump ATPase. However, little is known about regulation of the transmitter pool size, particularly in regard to amino acid neurotransmitters. We previously provided evidence for the existence of a potent endogenous inhibitory protein factor (IPF), which causes reduction of glutamate and GABA accumulation into isolated, purified synaptic vesicles. In this study we demonstrate that IPF is concentrated most in the synaptosomal cytosol fraction and that, when introduced into the synaptosome, it leads to a decrease in calcium‐dependent exocytotic (but not calcium‐independent) release of glutamate in a concentration‐dependent manner. In contrast, α‐fodrin (non‐erythroid spectrin), which is structurally related to IPF and thought to serve as the precursor for IPF, is devoid of such inhibitory activity. Intrasynaptosomal IPF also caused reduction in exocytotic release of GABA and the monoamine neurotransmitter serotonin. Whether IPF affects vesicular storage of multiple neurotransmittersin vivowould depend upon the localization of IPF. These results raise the possibility that IPF may modulate synaptic transmission by acting as a quantal size regulator of one or more neurotransmitters.