银杏内酯B对大鼠下丘脑室旁核神经元自发放电的影响

目的研究银杏内酯B（GinkgolideB，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％1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（GinkgolideB，BN520211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。

Effects of ginkgolide B on neuronal discharges in paraventricular nucleus of rat hypothalamic slices

Objective To study the central role of ginkgolide B （BN52021） in regulating cardiovascular function of nerve center by examining the effects of ginkgolide B on the electrical activity of rat paraventricular nucleus （PVN） neurons in hypothalamic slice preparation and to elucidate the mechanism involved. Methods Extracellular single-unit discharge recording technique. Results （1） In response to the application of ginkgolide t3 （0.1, 1, 10 μmol/L; n = 27） into the perfusate for 2 rain, the spontaneous discharge rates （SDR） of 26 （26/27, 96.30%） neurons were significantly decreased in a dose-dependent manner. （2） Pretreatment with L-glutamate （L-Glu, 0.2 mmol/L） led to a marked increase in the SDR of all 8 （100%） neurons in an epileptiform pattern. The increased discharges were suppressed significantly after ginkgolide B （1 μmol/L） was applied into the perfusate for 2 min. （3） In 8 neurons, perfusion of the selective L-type calcium channel agonist, Bay K 8644 （0.1 μmol/L）, induced a significant increase in the discharge rates of 8 （8/8, 100%） neurons, while ginkgolide B （1μmol/L） applied into the perfusate, could inhibit the discharges of 8 （100%） neurons. （4） In 8 neurons, the broad potassium channels blocker, tetraethylammonium （TEA, 1 mmol/L） completely blocked the inhibitory effect of ginkgolide B （1 μmol/L）. Conclusion These results suggest that ginkgolide B can inhibit the electrical activity of paraventricular neurons. The inhibitory effect may be related to the blockade of L-type voltage-activated calcium channel and potentially concerned with delayed rectifier potassium channel （KDR）.