Alger B E, Nicoll R A
Science. 1980 Dec 5;210(4474):1122-4. doi: 10.1126/science.7444438.
Synaptic excitation of hippocampal cells during blockade of synaptic inhibition results in an epileptiform "burst" potential followed by a prolonged afterhyperpolarization. This afterhyperpolarization resembles the one that is seen after the epileptic interictal spike and that is considered of critical importance in preventing seizure development. The afterhyperpolarization produced in the presence of y-aminobutyric acid antagonists is associated with a conductance increase and is inhibitory. It can occur in an all-or-none fashion after a burst, is independent of chloride, and is depressed by barium. The afterhyperpolarization has a reversal potential of (-86) millivolts, and the reversal potential is strongly dependent on the extracellular concentration of potassium. The afterhyperpolarization appears to be an intrinsic, inhibitory potassium potential mediated by calcium. This finding has implications for understanding the cellular mechanisms of epilepsy.
在突触抑制被阻断期间，海马细胞的突触兴奋会导致癫痫样“爆发”电位，随后是长时间的超极化后电位。这种超极化后电位类似于癫痫发作间期棘波后出现的超极化后电位，并且被认为在预防癫痫发作发展中至关重要。在γ-氨基丁酸拮抗剂存在的情况下产生的超极化后电位与电导增加相关且具有抑制性。它可以在爆发后以全或无的方式出现，与氯离子无关，并被钡抑制。超极化后电位的反转电位为（-86）毫伏，且该反转电位强烈依赖于细胞外钾离子浓度。超极化后电位似乎是一种由钙介导的内在抑制性钾离子电位。这一发现对于理解癫痫的细胞机制具有重要意义。
