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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >alpha-Latrotoxin affects mitochondrial potential and synaptic vesicle proton gradient of nerve terminals.
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alpha-Latrotoxin affects mitochondrial potential and synaptic vesicle proton gradient of nerve terminals.

机译：α-Lato毒素影响神经末梢的线粒体电位和突触小泡质子梯度。

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摘要

Ca(2+)-independent [(3)H]GABA release induced by alpha-latrotoxin was found to consist of two sequential processes: a fast initial release realized via exocytosis and more delayed outflow through the plasma membrane GABA transporters [Linetska, M.V., Storchak, L.G., Tarasenko, A.S., Himmelreich, N.H., 2004. Involvement of membrane GABA transporters in alpha-latrotoxin-stimulated [(3)H]GABA release. Neurochem. Int. 44, 303-312]. To characterize the toxin-stimulated events attributable to the transporter-mediated [(3)H]GABA release from rat brain synaptosomes we studied the effect of alpha-latrotoxin on membrane potentials and generation of the synaptic vesicles proton gradient, using fluorescent dyes: potential-sensitive rhodamine 6G and pH-sensitive acridine orange. We revealed that alpha-latrotoxin induced a progressive dose-dependent depolarization of mitochondrial membrane potential and an irreversible run-down of the synaptic vesicle proton gradient. Both processes were insensitive to the presence of cadmium, a potent blocker of toxin-formed transmembrane pores, indicating that alpha-latrotoxin-induced disturbance of the plasma membrane permeability was not responsible to these effects. A gradual dissipation of the synaptic vesicle proton gradient closely coupled with lowering the vesicular GABA transporter activity results in a leakage of the neurotransmitter from synaptic vesicles to cytoplasm. As a consequence, there is an essential increase in GABA concentration in a soluble cytosolic pool that appears to be critical parameter for altering the mode of the plasma membrane GABA transporter operation from inward to outward. Thus, our data allow clarifying what cell processes underlain a recruitment of the plasma membrane transporter-mediated pathway in alpha-LTX-stimulated secretion.
机译：Ca-（2+）独立的[（3）H] GABA释放由α-latrotoxin诱导被发现包括两个顺序的过程：通过胞吐作用实现的快速初始释放和通过质膜GABA转运蛋白的更多延迟流出[Linetska，MV ，Storchak，LG，Tarasenko，AS，新罕布什尔州希默勒里希，2004年。膜GABA转运蛋白参与α-拉托毒素刺激的[（3）H] GABA释放。神经化学。诠释44，303-312]。为了表征可归因于大鼠脑突触小体中转运蛋白介导的[（3）H] GABA释放的毒素刺激事件，我们使用荧光染料研究了α-拉毒素对膜电位和突触小泡质子梯度产生的影响。罗丹明6G和pH敏感a啶橙。我们发现，α-lato毒素诱导线粒体膜电位的逐步剂量依赖性去极化和突触小泡质子梯度的不可逆转的下降。这两个过程都对镉的存在不敏感，镉是毒素形成的跨膜孔的有效阻滞剂，表明α-拉托毒素诱导的质膜通透性障碍与这些作用无关。突触小泡质子梯度的逐渐消散与降低小泡的GABA转运蛋白活性紧密相关，导致神经递质从突触小泡泄漏到细胞质。结果，可溶性胞质池中的GABA浓度显着增加，这似乎是改变质膜GABA转运蛋白从内向外运行方式的关键参数。因此，我们的数据可以阐明在α-LTX刺激的分泌中募集质膜转运蛋白介导的途径的细胞过程。

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