Schwartzkroin P A, Prince D A
Brain Res. 1980 Mar 3;185(1):169-81. doi: 10.1016/0006-8993(80)90680-0.
The effects of the potassium channel blockers, tetraethylammonium (TEA) and tetramethylammonium (TMA) on behavior of hippocampal CA1 neurons were studied in the in vitro slice preparation. Intracellular injections of TEA produced marked spike broadening, increased input resistance, and a prolongation of a putative slow calcium-activated afterhyperpolization (AHP). Little effect was seen on synaptic potentials. Bursting activity induced by TEA in hippocampal neurons was qualitatively different from the epileptiform bursting induced by raising extracellular potassium concentrations or by including penicillin in the bathing medium. Effects of TMA were qualitatively similar to those of TEA, but much slower and less dramatic. The results suggested that there were at least two different potassium channels in the membranes of hippocampal CA1 neurons, and that both were important in determining normal neuronal activity. TEA appeared to preferentially block a fast, voltage-dependent potassium conductance (gk); however, it also modified the slow, calcium-activated gk. Although cell bursting activity may have resulted from blockade of a gk produced by TEA treatment, the epileptiform bursts produced by penicillin exposure appeared to be independent of this mechanism.
在体外脑片制备中研究了钾通道阻滞剂四乙铵（TEA）和四甲铵（TMA）对海马CA1神经元行为的影响。细胞内注射TEA可导致明显的动作电位增宽、输入电阻增加以及假定的慢钙激活后超极化（AHP）延长。对突触电位影响较小。TEA在海马神经元中诱导的爆发活动在性质上不同于通过提高细胞外钾浓度或在浴液中加入青霉素诱导的癫痫样爆发。TMA的作用在性质上与TEA相似，但作用更慢且不那么显著。结果表明，海马CA1神经元膜上至少存在两种不同的钾通道，且两者在决定正常神经元活动中都很重要。TEA似乎优先阻断快速的电压依赖性钾电导（gk）；然而，它也改变了慢的钙激活gk。虽然细胞爆发活动可能是由TEA处理导致的gk阻断引起的，但青霉素暴露产生的癫痫样爆发似乎与该机制无关。
