Sawano H
Department of Oral Physiology, School of Dentistry, Iwate Medical University, Japan.
Nihon Seirigaku Zasshi. 1990;52(11):363-73.
Effects of NaF on the synaptic transmission of bullfrog sympathetic ganglia were studied by extra- and intracellular recordings. The results obtained were as follows: 1) The amplitude of the orthodromic compound action potential (CAP) evoked by preganglionic nerve stimulation was remarkably augmented with 10 microM NaF, whereas that of the antidromic CAPs remained unchanged with the same dose of NaF. The low amplitude of the orthodromic CAP which was diminished by a low-Ca2(+)-ringer's solution reversed with an additional administration of NaF. The amplitudes of the orthodromic CAPs were enhanced by phosphodiesterase inhibitors such as isobutylmethylxanthine, theophylline, and physostigmine. In addition, augmentation of the orthodromic CAPs was induced by an adenylate cyclase activator (forskolin) and d.b-cAMP; however, its augmented responses were not affected by an additional administration of NaF. 2) In the intracellular recording, NaF showed no effect on the resting membrane potential and depolarizing response induced by acetylcholine. However, the EPSP appearing in the phase of afterhyperpolarization of the orthodromic action potential was significantly increased by NaF, whereas no effect was found on the antidromic action potential. In order to evaluate these findings, effects of NaF on the decreased low-Ca2(+)-action potential were observed. After application of NaF, the low-Ca2(+)-orthodromic EPSPs were reversed, and when the height of the EPSP was raised to the critical firing level, a spike potential was driven in the cell. These facts suggest that the site of NaF action seems to exist in the presynaptic rather than postsynaptic process. Furthermore, it suggests that NaF probably acts on Gs-protein which activates adenylate cyclase at the presynaptic membrane. This resulted in a great increase in intracellular cAMP at the synaptic terminal and it triggered the Ca2(+)-increase. As an inevitable consequence, release of transmitter from the nerve terminals of the frog sympathetic ganglion was finally facilitated. These factors supposedly resulted in augmentation of the amplitude of the orthodromic CAP.
通过细胞外和细胞内记录研究了氟化钠对牛蛙交感神经节突触传递的影响。获得的结果如下：1）用10微摩尔的氟化钠时，节前神经刺激诱发的顺向复合动作电位（CAP）的幅度显著增大，而相同剂量的氟化钠对逆向CAP的幅度没有影响。低钙林格氏液降低的顺向CAP的低幅度，在额外给予氟化钠后逆转。顺向CAP的幅度被磷酸二酯酶抑制剂如异丁基甲基黄嘌呤、茶碱和毒扁豆碱增强。此外，腺苷酸环化酶激活剂（福斯高林）和二丁酰环磷腺苷（d.b-cAMP）可诱导顺向CAP增大；然而，其增大的反应不受额外给予氟化钠的影响。2）在细胞内记录中，氟化钠对静息膜电位和乙酰胆碱诱导的去极化反应没有影响。然而，氟化钠使顺向动作电位后超极化阶段出现的兴奋性突触后电位（EPSP）显著增加，而对逆向动作电位没有影响。为了评估这些发现，观察了氟化钠对降低的低钙动作电位的影响。应用氟化钠后，低钙顺向EPSP逆转，当EPSP的幅度升高到临界发放水平时，细胞中引发了一个锋电位。这些事实表明，氟化钠的作用位点似乎存在于突触前而非突触后过程中。此外，这表明氟化钠可能作用于突触前膜上激活腺苷酸环化酶的Gs蛋白。这导致突触末端细胞内cAMP大量增加，并引发钙离子增加。作为必然结果，最终促进了蛙交感神经节神经末梢递质的释放。这些因素可能导致顺向CAP幅度增大。
