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目的研究三羟异黄酮(GENISTEIN,GST)对静息状态下的海马脑片神经元活动的影响。方法应用细胞外记录单位放电技术。结果 (1)在48个CA1区神经元放电单位给予GST(10,50,100 ΜMOL／L)2 MIN,有46个放电单位(95．83％)放电频率明显降低,且呈剂量依赖性;(2)在9个CA1区神经元放电单位上,GST(50ΜMOL／ L)的抑制效应可被G蛋白激活的内向整流型钾通道(G PROTEIN-COUPLED INWARDLY RECTIFYING K+ CHANNELS,GIRK)阻断剂(TETRAETHYLAMMONIUM,TEA)1 MMOL／L完全阻断;(3)10个放电单位灌流一氧化氮合酶抑制剂(NG-NITRO-L-ARGININE METHYL ESTER,L-NAME)50ΜMOL／L,有9个单位(90．0％)放电明显增加,在此基础上灌流GST(50 ΜMOL／L)2 MIN,放电被抑制;(4)预先用0．2 MMOL／L的L-GLUTAMATE(L-GLU)灌流海马脑片,11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GST(50ΜMOL／L)2 MIN,其癫痫样放电被抑制。结论 GST可抑制海马神经元自发放电,并可抑制由L-NAME和L-GLUTAMATE诱发的神经元放电。提示GST对中枢神经元通过降低其活动而具有一定程度的保护作用,这种作用与钾电流有关,似与其激动GIRK促进K+外流引起细胞膜超极化以及NO 产生增加有关。
Objective To investigate the effect of genistein (GST) on neuronal activity in hippocampal slices at rest. Methods Extracellular recording unit discharge technique was used. Results (1) The discharge frequency of GST (10, 50, 100 ΜMOL / L) 2 MIN in 48 CA1 neurons was significantly reduced at 46 discharge units (95.83%) in a dose dependent manner. (2) ) The inhibitory effect of GST (50 MOL / L) on the neuronal discharge units of 9 CA1 neurons can be blocked by the G protein-activated potassium channel (G PROTEIN-COUPLED INWARDLY RECTIFYING K + CHANNELS, GIRK) blocker (TETRAETHYLAMMONIUM, TEA) 1 MMOL / L completely blocked; (3) 10 units of perfusion nitric oxide synthase inhibitor (NG-NITRO-L-ARGININE METHYL ESTER, L-NAME) .0%) discharge increased significantly, on the basis of GST (50 ΜMOL / L) 2 MIN, discharge was inhibited; (4) 0.2 MMOL / L of L-GLUTAMATE The discharge frequency of eleven discharge units increased significantly, showing epileptiform discharge. On this basis, GST (50 MOL / L) 2 MIN was infused and the epileptiform discharge was inhibited. Conclusion GST can inhibit the spontaneous discharge of hippocampal neurons and inhibit the neuronal firing induced by L-NAME and L-GLUTAMATE. It is suggested that GST may protect central nervous system to a certain extent by reducing its activity, which is related to potassium current, which may be related to its activation of GIRK and K + efflux to cause hyperpolarization of cell membrane and increase of NO production.