ffrench-Mullen J M, Rogawski M A, Barker J L
Laboratory of Neurophysiology, National Institute of Neurological and Communicative Disorders and Stroke, Bethesda, MD 20892.
Neurosci Lett. 1988 Jun 7;88(3):325-30. doi: 10.1016/0304-3940(88)90232-7.
We studied the effects of phencyclidine (PCP) on voltage-dependent K+ currents in cultured embryonic rat hippocampal neurons. Whole cell voltage-clamp recordings were made in the presence of tetrodotoxin to block Na+ current. Depolarizing voltage steps activated two outward current components: (i) a rapidly activating and inactivating ('transient') component, IA, and (ii) a slowly activating, minimally inactivating ('sustained'), component, IK. At low concentrations (less than 50-100 microM), PCP produced a selective, reversible blockade of IK with minimal effect on IA; however, at higher concentrations both currents were suppressed. The IC50's for blockade of IK and IA were 36 and 310 microM, respectively.
我们研究了苯环己哌啶(PCP)对培养的胚胎大鼠海马神经元电压依赖性钾离子电流的影响。在存在河豚毒素以阻断钠离子电流的情况下进行全细胞电压钳记录。去极化电压阶跃激活了两个外向电流成分:(i)一个快速激活和失活(“瞬时”)成分,IA,以及(ii)一个缓慢激活、最小失活(“持续”)成分,IK。在低浓度(小于50 - 100微摩尔)时,PCP对IK产生选择性、可逆性阻断,对IA影响最小;然而,在较高浓度时,两种电流均被抑制。IK和IA阻断的半数抑制浓度(IC50)分别为36和310微摩尔。