Koketsu K, Yamamoto K
Br J Pharmacol. 1974 Jan;50(1):69-77. doi: 10.1111/j.1476-5381.1974.tb09594.x.
1 The mode of action of lithium on electrical activity in the sympathetic ganglia of the bullfrog has been studied by recording extracellular and intracellular potential changes. Changes in nerve conduction and various types of synaptic transmission were studied when sodium ions in the external solution were totally replaced by equimolar concentrations of lithium ions and also when lithium ions were added to the external Ringer solution.2 Nerve conduction and nicotinic transmission in sympathetic ganglia were completely blocked in sodium-free sucrose solution, but were restored when the preparations were transferred to a sodium-free lithium solution.3 In the sodium-free lithium solution, the slow excitatory postsynaptic potential (e.p.s.p.) and muscarinic acetylcholine-depolarization were restored while the slow inhibitory postsynaptic potential (i.p.s.p.) and the muscarinic acetylcholine-hyperpolarization were not restored. Furthermore, the early after-discharges were accelerated and the inhibition of after-discharges was eliminated. These results support the hypothetical concept that the slow i.p.s.p. is generated by an activation of the electrogenic sodium pump.4 In the sodium-free lithium solution, restoration of nerve conduction and synaptic transmission were transient phenomena; both conduction and transmission were gradually blocked when preparations were soaked in the solution for long periods. The blockade appeared to be due to membrane depolarization.5 When lithium ions (20 mM) were added to the Ringer solution, nicotinic transmission was depressed. The slow e.p.s.p. was also depressed, but less so than the slow i.p.s.p. The early after-discharge was, however, accelerated; presumably due to the marked depression of the slow i.p.s.p. in this solution.6 Changes in synaptic transmission in Ringer solution containing lithium ions could be explained by membrane depolarization, a reduction of acetylcholine release and a depression of the electrogenic sodium pump.7 All results obtained in the present experiments could be explained by supposing that lithium ions are able to substitute for sodium ions in passive ionic membrane transport dependent on electrochemical energy but not in active ionic membrane transport dependent on metabolic energy.
1 通过记录细胞外和细胞内电位变化,研究了锂对牛蛙交感神经节电活动的作用方式。当外部溶液中的钠离子被等摩尔浓度的锂离子完全替代时,以及当锂离子添加到外部林格溶液中时,研究了神经传导和各种类型突触传递的变化。
2 在无钠蔗糖溶液中,交感神经节中的神经传导和烟碱传递完全被阻断,但当制剂转移到无钠锂溶液中时恢复。
3 在无钠锂溶液中,慢兴奋性突触后电位(e.p.s.p.)和毒蕈碱型乙酰胆碱去极化恢复,而慢抑制性突触后电位(i.p.s.p.)和毒蕈碱型乙酰胆碱超极化未恢复。此外,早期放电后活动加速,放电后抑制消除。这些结果支持了这样一个假设概念,即慢i.p.s.p.是由电生钠泵的激活产生的。
4 在无钠锂溶液中,神经传导和突触传递的恢复是短暂现象;当制剂长时间浸泡在溶液中时,传导和传递都会逐渐被阻断。这种阻断似乎是由于膜去极化。
5 当将锂离子(20 mM)添加到林格溶液中时,烟碱传递受到抑制。慢e.p.s.p.也受到抑制,但程度小于慢i.p.s.p.。然而,早期放电后活动加速;推测是由于该溶液中慢i.p.s.p.的显著抑制。
6 含锂离子的林格溶液中突触传递的变化可以用膜去极化、乙酰胆碱释放减少和电生钠泵的抑制来解释。
7 本实验获得的所有结果可以通过假设锂离子能够在依赖电化学能量的被动离子膜转运中替代钠离子,但不能在依赖代谢能量的主动离子膜转运中替代钠离子来解释。