丹参酮ⅡA 预防慢性缺氧大鼠认知功能障碍的电生理机制

目的:探讨丹参酮ⅡA(TⅡA)预防慢性缺氧大鼠认知功能障碍的电生理机制。方法:将18只雄性SD大鼠(200-250 g)随机分为对照组、模型组(Model组)、TⅡA(10mg/kg.d)治疗组(TⅡA组)。复制慢性缺氧大鼠认知功能障碍模型,并给予相应治疗,在脑片水平运用膜片钳技术检测海马CA1区的LTP变化,并检测海马CA1区锥体细胞的兴奋性变化。结果:(1)给予高频强直刺激(HFS)后各组兴奋性突出后电位(fEPSP)斜率均显著增加,即均可诱发LTP并持续1h以上,但模型组LTP较对照组显著减弱(P<0.05),TⅡA治疗组LTP较模型组明显增强(P<0.05);(2)慢性缺氧使海马CA1锥体细胞放电所需的刺激电流幅度显著增加、阈电位升高、兴奋性降低,同样刺激强度条件下动作电位数量减少,TⅡA干预可明显减轻慢性缺氧对海马CA1锥体细胞的上述抑制。结论:TⅡA可能是通过维持海马CA1锥体细胞的兴奋性、维持海马的突出可塑性减轻慢性缺氧对认知功能的损害。

The Electrophysiological Mechanism of Tanshinone ⅡA Preventing Chronic Hypobaric Hypoxia-Induced Cognitive Deficits

Objective: To investigate the electrophysiological mechanism of Tanshinone ⅡA(TⅡA) preventing cognitive deficits induced by chronic hypobaric hypoxia.Methods: Eighteen male Sprague-Dawley rats(200-250 g) were randomly divided into three groups(n=6): Control group,Model group and TⅡA group.Hippocampal CA1 LTP was detected by patch-clamp recordings in rat brain slices.Excitability of Hippocampal CA1 pyramidal neurons was measured by whole-cell patch-clamp recordings.Results: The LTP of hippocampal CA1 was inhibitted by chronic hypobaric hypoxia,and TⅡA can maintain the LTP.The decrease of excitability of hip-pocampal CA1 pyramidal neurons caused by chronic hypobaric hypoxia was markedly improved by TⅡA.Conclusions: TⅡA can pre-vent cognitive deficits caused by chronic hypobaric hypoxia via maintaining the excitability of hippocampal CA1 pyramidal neurons.