Men'shikova E V, Tverdislova I L, Bratkovskaia L B, Glebov R N, Ritov V B
Biokhimiia. 1989 Jul;54(7):1059-65.
Using the fluorescent probes, Quin 2 and chlortetracycline, a comparative study of the Ca2+ and inositol-1.4.5-triphosphate (IP3)-induced Ca2+ release from rabbit skeletal muscle sarcoplasmic reticulum (SR) terminal cisterns and rat brain microsomal vesicles was carried out. It was shown that Ca2+ release from rat brain microsomal vesicles is induced both by IP3 and Ca2+, whereas that in SR terminal cisterns is induced only by Ca2+. Data from chlorotetracycline fluorescence analysis revealed that CaCl2 (50 microM) causes the release of 15-20% and 40-50% of the total Ca2+ pool accumulated in rat brain microsomal vesicles and rabbit SR terminal cisterns, respectively. Using Quin 2, it was found that IP3 used at the optimal concentration (1.5 mM) caused the release of 0.4-0.6 nmol of Ca2+ per mg microsomal protein, which makes up to 10-15% of the total Ca2+ pool. IP3 does not induce Ca2+ release in SR. Preliminary release of Ca2+ from brain microsomes induced by IP3 diminishes the liberation of this cation induced by Ca2+. It is suggested that brain microsomes contain a Ca2+ pool which is exhausted under the action of the both effectors, Ca2+ and IP3.
利用荧光探针喹啉-2和金霉素，对兔骨骼肌肌浆网（SR）终池和大鼠脑微粒体囊泡中Ca2+及肌醇-1,4,5-三磷酸（IP3）诱导的Ca2+释放进行了比较研究。结果表明，大鼠脑微粒体囊泡中的Ca2+释放可由IP3和Ca2+诱导，而SR终池中的Ca2+释放仅由Ca2+诱导。金霉素荧光分析数据显示，CaCl2（50 microM）分别导致大鼠脑微粒体囊泡和兔SR终池中积累的总Ca2+池释放15%-20%和40%-50%。使用喹啉-2发现，以最佳浓度（1.5 mM）使用的IP3导致每毫克微粒体蛋白释放0.4-0.6 nmol的Ca2+，占总Ca2+池的10%-15%。IP3不会在SR中诱导Ca2+释放。IP3诱导的大鼠脑微粒体中Ca2+的初步释放会减少Ca2+诱导的该阳离子的释放。提示脑微粒体含有一个Ca2+池，在Ca2+和IP3这两种效应物的作用下会耗尽。
