Curtis B M, Scurlock J E
Anesthesiology. 1981 Apr;54(4):270-7. doi: 10.1097/00000542-198104000-00003.
Tetraethylammonium (TEA+) derivatives in which one of the ethyl groups is replaced by a longer chain alkane (C4-C16) were tested for their ability to block the compound action potential (CAP) of frog sciatic nerve. A parabolic relation between chain length and 100 per cent blocking dose was found, suggesting an optimal size of C12 for the inhibitory receptor. Two types of inhibition were observed. Type 1 was an inhibition of the CAP at all frequencies when the nerve was perfused with the TEA+ derivative. Interaction with tetrodotoxin suggests this is a Na+ channel effect. Type 2 was an irreversible (still present after nerve wash) frequency-dependent inhibition that is distinct from and synergistic with Na+ channel blocking local anesthetics. From the kinetics of inhibition onset and transport studies, it is suggested that the ultralong action of the TEA+ derivatives is mediated by binding to a receptor at the internal part of K+ channels.
测试了其中一个乙基被更长链烷烃（C4 - C16）取代的四乙铵（TEA +）衍生物阻断青蛙坐骨神经复合动作电位（CAP）的能力。发现链长与100%阻断剂量之间呈抛物线关系，表明抑制性受体的最佳大小为C12。观察到两种类型的抑制。类型1是当神经用TEA +衍生物灌注时，在所有频率下对CAP的抑制。与河豚毒素的相互作用表明这是一种Na +通道效应。类型2是一种不可逆的（神经冲洗后仍存在）频率依赖性抑制，与Na +通道阻断局部麻醉药不同且具有协同作用。从抑制起始动力学和转运研究来看，表明TEA +衍生物的超长作用是通过与K +通道内部的受体结合介导的。
