Kyriakides M A, Sawyer R T, Allen S L, Simpson M G
Neuropharm Ltd., Hendy, Dyfed, U.K.
Toxicol Lett. 1990 Oct;53(3):285-95. doi: 10.1016/0378-4274(90)90233-c.
The effects of triethyltin (TET) have been examined using intracellular electrophysiological recording techniques from identified neurons of the leech (Hirudo medicinalis) CNS and from salivary glands of the giant Amazon leech (Haementeria ghilianii). TET, at concentrations as low as 10(-5) M, caused a reversible neuronal membrane depolarisation accompanied by an increase in firing frequency of action potentials (which could lead to conduction block at 10(-4) M) and a concomitant decrease in membrane resistance. TET-induced membrane depolarisation still occurred in saline where Na+, K+ and Ca2+ had been replaced by choline. TET decreased the rate of the depolarising and repolarising phases of the action potential. This also occurred in Haementeria salivary gland cells, in which the only inward cation channel is a calcium channel. The calcium channel blocker, manganese, did not block the effects of TET. TET counteracted the effects on the action potential of the potassium channel blocker, tetraethylammonium chloride (TEA). TET-induced neurotoxicity occurred independently of any resultant toxic effects on the myelin sheath. The action of TET is consistent with our view that it causes an increase of intracellular free Ca2+ probably via release from intracellular stores and inhibition of Ca2+ reuptake. A resulting inhibition of the Na+/K+ and Ca2+ pumps may also occur.
已使用细胞内电生理记录技术，对来自水蛭（医用水蛭）中枢神经系统的特定神经元以及巨型亚马逊水蛭（盖氏巨蛭）唾液腺的三乙锡（TET）效应进行了研究。低至10⁻⁵ M浓度的TET，可引起可逆的神经元膜去极化，同时伴有动作电位发放频率增加（在10⁻⁴ M时可导致传导阻滞）以及膜电阻随之降低。在Na⁺、K⁺和Ca²⁺被胆碱取代的盐溶液中，TET诱导的膜去极化仍会发生。TET降低了动作电位去极化和复极化阶段的速率。这在盖氏巨蛭唾液腺细胞中也会发生，其中唯一的内向阳离子通道是钙通道。钙通道阻滞剂锰并不能阻断TET的作用。TET抵消了钾通道阻滞剂氯化四乙铵（TEA）对动作电位的影响。TET诱导的神经毒性独立于对髓鞘的任何由此产生的毒性作用而发生。TET的作用与我们的观点一致，即它可能通过从细胞内储存库释放Ca²⁺并抑制Ca²⁺再摄取，从而导致细胞内游离Ca²⁺增加。还可能由此抑制Na⁺/K⁺泵和Ca²⁺泵。
