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目的研究银杏内酯B(Ginkgolide B,BN52021)对静息状态下的下丘脑脑片室旁核神经元自发放电活动的影响。方法应用细胞外记录单位放电技术。结果(1)在27个下丘脑室旁核神经元放电单位给予银杏内酯B(0.1,1,10μmol/L)2分钟,有26个放电单位(96.30%)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)灌流下丘脑脑片,8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)2分钟,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个下丘脑脑片,8个放电单位(100%)全部放电增加,在此基础上灌流银杏内酯B(1μmol/L)2分钟,8个放电单位(100%)放电频率明显减低;(4)在8个下丘脑室旁核神经元放电单位上,银杏内酯B(1μmol/L)的抑制效应可被广泛钾通道阻断剂(tetraethylammonium,TEA)1mmol/L完全阻断。结论银杏内酯B(Ginkgolide B,BN52021)可抑制下丘脑室旁核神经元自发放电,并可抑制由L-glutamate诱发的神经元放电。提示银杏内酯B对心血管中枢神经元通过降低其活动而具有一定程度的保护作用,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。
Objective To investigate the effect of Ginkgolide B (BN52021) on the spontaneous discharge of neurons in the paraventricular nucleus of the hypothalamic slice under resting conditions. Methods The application of extracellular recording unit discharge technology. Results (1) In 27 hypothalamic nucleus paraventricular nucleus discharge units given ginkgolide B (0.1, 1, 10 μmol/L) for 2 minutes, the discharge frequency of 26 discharge units (96.30%) was significantly reduced and dose Dependence; (2) Hypothalamic brain slices were perfused with 0.2 mmol/L L-glutamate (L-Glu) in advance, the discharge frequency of 8 discharge units was significantly increased, manifested as epileptiform discharge, and ginkgo lactone was perfused on this basis. B (1μmol/L) for 2 minutes, all epileptiform discharges were inhibited; (3) Eight hypothalamic brain slices were perfused with the L-type calcium channel opener BayK8644 in advance, and all discharges in 8 discharge units (100%) increased. On this basis, Ginkgolide B (1μmol/L) perfusion for 2 minutes, the discharge frequency of 8 discharge units (100%) was significantly reduced; (4) Ginkgolide B in 8 hypothalamic paraventricular nucleus discharge units. The inhibitory effect of (1 μmol/L) can be completely blocked by 1 mmol/L of tetraethylammonium (TEA). Conclusion Ginkgolide B (BN52021) inhibits the spontaneous discharge of hypothalamic paraventricular nucleus neurons and inhibits the neuronal firing induced by L-glutamate. It is suggested that ginkgolide B has a certain degree of protective effect on cardiovascular central neurons by reducing their activity. This effect may be related to the inhibition of L-type calcium channels by ginkgolide B, and may be associated with delayed rectifier potassium channels (delayed rectifier). Potassium channel, KDR) related.