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为了研究银杏内酯B(Ginkgolide B,BN52021)对静息状态下的海马脑片神经元活动的影响。本研究应用细胞外记录单位放电技术观察了银杏内酯B对海马神经元电活动的影响,并分析了相关机制。结果显示:(1)在43个CA1区神经元放电单位给予银杏内酯B(0.1,1,10μmol/L)2min,有42个放电单位(97.67%)放电频率明显降低,且呈剂量依赖性;(2)预先用0.2mmol/L的L-glutamate(L-Glu)灌流海马脑片,10个放电单位放电频率明显增加,表现为癫痫样放电,在此基础上灌流银杏内酯B(1μmol/L)2min,其癫痫样放电全部被抑制;(3)预先用L型钙通道开放剂BayK8644灌流8个海马脑片神经元,8个单位(100%)放电全部增加,在此基础上灌流银杏内酯B(1μmol/L)2min,7个放电单位(87.5%)放电频率明显减低;(4)在8个CA1区神经元,银杏内酯B(1μmol/L)对单位放电的抑制效应可被1mmol/L广泛钾通道阻断剂(tetraethylammonium,TEA)完全阻断。上述结果提示,银杏内酯B可抑制海马CA1区神经元的自发放电,这种作用可能与银杏内酯B抑制L型钙通道有关,而且可能与延迟整流型钾通道(delayed rectifier potassium channel,KDR)有关。银杏内酯B通过降低神经元的活动而发挥对中枢神经元的保护作用。
In order to investigate the effect of Ginkgolide B (BN52021) on neuronal activity in resting hippocampal slices. In this study, the extracellular recording unit discharge technique was used to observe the effect of Ginkgolide B on the electrical activity of hippocampal neurons. The relevant mechanism was also analyzed. The results showed that: (1) The firing rate of 42 discharge units (97.67%) was significantly decreased in 43 CA1 neurons with Ginkgolide B (0.1,1,10 μmol / L) for 2 min and in a dose-dependent manner ; (2) The perfusion of hippocampal slices with 0.2 mmol / L L-glutamate in advance, the discharge frequency of 10 discharge units increased obviously, showing epileptiform discharge. On the basis of perfusion ginkgolide B (1 μmol / L) for 2 min, all of which were inhibited by epileptiform discharge. (3) Eight hippocampal neurons were pre-perfused with BayK8644 L-type calcium channel opener, and all eight units (100% (4) The inhibitory effect on the unit discharge of neurons and ginkgolide B in 8 CA1 areas (1μmol / L) for 2min and 7 discharge units (87.5% It can be completely blocked by 1 mmol / L tetraethylammonium (TEA). The above results suggest that Ginkgolide B can inhibit spontaneous discharge of neurons in hippocampal CA1 region, which may be related to the inhibition of L-type calcium channel by Ginkgolide B, and may be related to the delayed rectifier potassium channel (KDR )related. Ginkgolide B exerts a central neuronal protective effect by decreasing neuronal activity.