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作 者:林悦[1] 王茹[1] 王昕[1] 何瑞荣[1] 武宇明[1]
机构地区:[1]河北医科大学基础医学研究所生理学教研室,石家庄050017
出 处:《神经解剖学杂志》2009年第1期68-73,共6页Chinese Journal of Neuroanatomy
摘 要: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。Extracellular single-unit discharge recording technique was used to examine the effects of Ginkgolide B ( BN52021 ) on the discharges of neurons in CA1 area of hippocampal slices and to elucidate the mechanisms involved. The results showed that : ( 1 ) In response to the application of ginkgolide B (0.1, 1, 10 μmol/L; n = 43) into the perfusate for 2 min, the spontaneous discharge rates (SDR) of 42/43 (97.67%) 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 10 ( 100% ) neurons in an epileptiform pattern. The increased discharges were suppressed significantly after ginkgolide B ( 1 μxmoL/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 rate of 8/8 (100%) neurons. Ginkgolide B (1μmol/L) applied into the perfusate inhibited the discharges of 7/8 (87.5%) slices; (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). These results suggest that ginkgolide B can inhibit the electrical activity of CAI neurons. The inhibitory effect may be related to the blockade of L-type voltage-activated calcium channel and may be concerned with delayed rectifier potassium channel (KDR), which indicated that ginkgolide B play a protective role on the central neurons.
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