Matsumoto M, Riker W K, Takashima K, Goss J R, Mela-Riker L
Eur J Pharmacol. 1985 Feb 26;109(2):213-8. doi: 10.1016/0014-2999(85)90422-4.
Synaptic transmission in the bullfrog sympathetic ganglion was studied by means of extra- and intracellular recordings. DMSO (3-10%) caused a single orthodromic stimulus to generate a brief burst of repetitive postganglionic discharges. DMSO also partially reversed a preexisting transmission failure in low Ca2+ medium. Ganglia were exposed to gradual reductions in extracellular Ca2+, in the absence and in the presence of DMSO. The recorded amplitude of the postganglionic compound action potential (CAP) was plotted as a function of Ca2+ concentration. In the absence of DMSO transmission failed progressively as Ca2+ was reduced from 1.8 to 0.47 mM but DMSO (3% and 10%) shifted the curve of transmission failure to the left (lower Ca2+ concentration). DMSO inhibits ganglion cholinesterase activity, but this is not the mechanism of its facilitatory effect on Ca2+ entry, since physostigmine did not shift the curve of transmission failure in low Ca2+ to the left. The data suggest that DMSO maintained transmitter release in low Ca2+ by a direct, nonspecific enhancement of Ca2+ influx into the presynaptic nerve terminal.
通过细胞外和细胞内记录的方法，对牛蛙交感神经节中的突触传递进行了研究。二甲基亚砜（DMSO，3 - 10%）使单个顺向刺激引发节后重复放电的短暂爆发。DMSO还部分逆转了低钙培养基中预先存在的传递失败。在不存在和存在DMSO的情况下，使神经节暴露于细胞外钙的逐渐减少中。将记录的节后复合动作电位（CAP）的幅度绘制为钙浓度的函数。在不存在DMSO的情况下，随着钙从1.8 mM降低到0.47 mM，传递逐渐失败，但DMSO（3%和10%）将传递失败曲线向左移动（更低的钙浓度）。DMSO抑制神经节胆碱酯酶活性，但这不是其对钙内流促进作用的机制，因为毒扁豆碱并未将低钙条件下的传递失败曲线向左移动。数据表明，DMSO通过直接、非特异性地增强钙流入突触前神经末梢，在低钙条件下维持递质释放。
