采用膜片钳内面向外式技术，在急性分离成年大鼠海马CAl区锥体细胞上记录到了外向整流氯离子通道（outwadly rectifving chloride channel, ORCC），长时间去极化（I>60mv）刺激后，在30%的游离膜片上记录到有外向整流特性的单通道氯电流，膜电位在-60mV到0mV之间的单通道电导为（16.58±1.54）Ps(n=10），而在0mv到+60mv之间电导为（40.92±3.17）pS，通道开放概率有明显的电压依赖性（膜电位-60mV时，P=0.44±0.12；膜电位为+60mv时，Pa=0.86±0.06，n=10），在对称C1-浓度（150 retool/L）时，通道翻转电位为（-4.17±1.84）mv。当溶液中部分NaCl被葡萄糖酸钠替代后，翻转电位为：（-34.23±4.86）mV（C1-1/[C1一]。-（30mmol/L）/（150 mmol/L）），接近氯离子通道的理论值，这表明通道具有氯离子选择性，浴槽液中分别加入氯通道阻断剂DIDS和SITS可以使+40mV的通道开放概率从（0.83±0.06）和（0.86±0.06）分别降低到（0.12±0.05）和（0.13±0.04）n=5)，冲洗后可使开放概率基本恢复，上述研究结果显示，在成年大鼠海马CAl神经元上存在外向整流氯离子通道。

The electrophysiological responses of CA3 pyramidal neurons and dentate granule (DG) cells in rat hippocampus were studied after transient forebrain ischemia using intracellular recording and staining techniques in vivo. Approximately 5 min of ischemic depolarization was induced using 4-vessel occlusion method. The spike threshold and rheobase of CA3 neurons remained unchanged up to 12h following reperfusion. No significant change in spike threshold was observed in DG cells but the rheobase transiently increased 6-9h after ischemia. The input resistance and time constant of CA3 neurons increased 0-3h after ischemia and returned to control ranges at later time periods. The spontaneous firing rate in CA3 neurons transiently decreased shortly following reperfusion, while that of DG cells progressively decreased after ischemia. In CA3 neurons, the amplitude and slope of excitatory postsynaptic potentials (EPSPs) transiently decreased 0-3h after reperfusion, and the stimulus intensity threshold for EPSPs transiently increased at the same time. No significant changes in amplitude and slope of EPSPs were observed in DG cells, but the stimulus intensity threshold for EPSPs slightly increased shortly after reperfusion. The present study demonstrates that the excitability of CA3 pyramidal neurons and DG cells after 5min ischemic depolarization is about the same as control levels, whereas the synaptic transmission to these cells was transiently suppressed after the ischemic insult. These results suggest that synaptic transmission is more sensitive to ischemia than membrane properties, and the depression of synaptic transmission may be a protective mechanism against ischemic insults.

KATP通道在细胞的新陈代谢与膜兴奋性的耦联中起重要作用，采用膜片钳的内面向外式记录方法，在成年大鼠海马cAl区锥体细胞上记录到一种被胞浆侧ATP和甲糖宁（tolbutarnide，一种KATP通道阻断剂）抑制的Ca2+依赖性钾离子通道，在细胞膜内外的K+浓度均为140mmol/L时，通道的电导为（204±21)f）pS，翻转电位为（3.57±1.13）mv，通道无整流性，通道开放概率及ATP对通道的抑制作用均呈现电压依赖性，该KATP通道与以往报道的“经典”KATP通道有显著不同，其活动受膜电位、胞内Ca2+和ATP三重调节，表明这是一种新型的KATP通道，上述结果表明在海马神经元上至少有两种性质不同的KAlP通道，提示神经元可能通过不同性质的KATP通道感受细胞内的代谢状态，进而调节细胞膜的兴奋性。

Using inside-out configuration of patch clamp techniques, ATP modulation of BKca channels was studied in hippocampal CAI pyramidal neurons of adult rat. Intracellular ATP application markedly increased BKca channel activity, and this ATP-produced increase in BK, channel activity was characterized by a higher opening frequency with no changes in channel open times. In the presence of specific inhibitor against protein kinase A, H-89, ATP did not induce any increase in the channel activity. Furthermore, adding H-89 after addition of ATP reversed the modulation produced by ATE In contrast, protein kinase C inhibitor chelerythrine exerted no apparent effects on ATP-induced channel activation. The present study suggests that BKca channels from hippocampal CA1 pyramidal neurons could be modulated by ATP via a functionally associated orotein kinase A-like orotein.

Buyang Huanwu Decoction (BYHWD), a traditional Chinese medicine, has been developed as a drug to be used for treatment of stroke for hundreds of years. However, the underlying mechanisms remain unknown. In the present study, the effects of BYHWD on delayed neuronal death of hippocampus after transient forebrain ischemia were examined in rats. Transient forebrain ischemia in a duration of 15 rain was induced with the four-vessel occlusion method. BYHWD (per 6.65g/kg) was given orally to rats twice each day for 7 days before ischemia. In BYHWD-pretreated rats, the neuronal injury in the hippocampal CA1 region was significantly less than that of controls. Oral administration of BYHWD also markedly attenuated the number of TUNEL-positive neurons and suppressed the expression of caspase-3p20, a product of catalytically active caspase-3, in the CA1 region. Our results suggest that an inhibition of caspase-3 and apoptosis by BYHWD may oartially account for its neuroorotection against ischemic iniury in the hippocampal CA1 region.