Gibbs M E, Ng K T
Brain Res Bull. 1976 Mar-Apr;1(2):203-8. doi: 10.1016/0361-9230(76)90070-8.
Diphenylhydantoin (DPH 10(-4)M) administered subcutaneously to chicks 5 min after a one-trial passive avoidance learning task successfully counteracted amnesia induced by pretreatment 5 min before learning with ouabain or cycloheximide (CXM). Biochemical assays confirmed that in chick forebrain homogenate DPH at concentrations of 1 and 5 X 10(-4)M enhanced Na+/K+ ATP'ase activity. Since both DPH and ouabain inhibit post-tetanic potentiation, the results support the hypothesis of an initial labile phase of memory based on sodium pump (Na+/K+ ATP'ase) activity. DPH was less effective in counteracting ouabain-induced amnesia if administered later than 10 min after learning and CXM-induced amnesia if administered later than 30 min after learning. This suggests that the effect of DPH on CXM-induced amnesia is through enhancement of Na+/K+ ATP'ase activity. It was suggested that the possible hyperpolarization of membrane potential associated with sodium pump activity may serve to mark the labile memory trace, enabling formation of a more permanent trace through protein synthesis.
在单次被动回避学习任务完成5分钟后，给雏鸡皮下注射苯妥英（DPH，10⁻⁴M），成功抵消了在学习前5分钟用哇巴因或环己酰亚胺（CXM）预处理所诱导的失忆。生化分析证实，在雏鸡前脑匀浆中，浓度为1×10⁻⁴M和5×10⁻⁴M的DPH可增强Na⁺/K⁺ ATP酶活性。由于DPH和哇巴因均抑制强直后增强，这些结果支持了基于钠泵（Na⁺/K⁺ ATP酶）活性的记忆初始不稳定阶段的假说。如果在学习后10分钟后给药，DPH在抵消哇巴因诱导的失忆方面效果较差；如果在学习后30分钟后给药，DPH在抵消CXM诱导的失忆方面效果较差。这表明DPH对CXM诱导的失忆的作用是通过增强Na⁺/K⁺ ATP酶活性实现的。有人提出，与钠泵活性相关的膜电位可能的超极化作用，可能有助于标记不稳定的记忆痕迹，从而通过蛋白质合成形成更持久的痕迹。
