Gandhi C R, Ross D H
Neurochem Res. 1987 Jan;12(1):67-72. doi: 10.1007/BF00971366.
Inositol 1,4,5-trisphosphate (IP3) was found to release Ca2+ from presynaptic nerve endings (synaptosomes) made permeable with saponin. ATP-dependent Ca2+ uptake was carried out until equilibrium was reached. Addition of IP3 produced a rapid release of Ca2+, which was complete within 60 sec, followed by Ca2+ reaccumulation to the original level in 5-7 min. Cholinergic receptor stimulation with muscarine also produced a similar Ca2+ release from synaptic endoplasmic reticulum. Ca2+ release by IP3 was not detectable in the absence of the mitochondrial inhibitors oligomycin or sodium azide. Reaccumulation of Ca2+ was prevented by the presence of vanadate, a potent inhibitor of Ca2+/Mg2+ ATPase. Half maximal and near complete release of Ca2+ took place at 0.4 microM and 3 microM IP3 concentrations, respectively. These studies demonstrate for the first time IP3 mobilization of Ca2+ from endoplasmic reticulum within synaptic plasma membranes.
肌醇1,4,5 -三磷酸（IP3）可使经皂角苷处理而具有通透性的突触前神经末梢（突触体）释放Ca2+。进行ATP依赖的Ca2+摄取直至达到平衡。加入IP3后会迅速释放Ca2+，60秒内释放完毕，随后在5 - 7分钟内Ca2+重新积累至原始水平。用毒蕈碱刺激胆碱能受体也会使突触内质网释放类似的Ca2+。在没有线粒体抑制剂寡霉素或叠氮化钠的情况下，无法检测到IP3引起的Ca2+释放。钒酸盐（一种Ca2+/Mg2+ ATP酶的有效抑制剂）的存在可阻止Ca2+的重新积累。Ca2+的半数最大释放和几乎完全释放分别发生在IP3浓度为0.4微摩尔和3微摩尔时。这些研究首次证明了IP3可从突触质膜内的内质网动员Ca2+。
