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。

短暂脑缺血可对随后的损伤性脑缺血表现出明显的耐受，有研究表明大电导ca2+依赖K+（BKCa）通道活动增强参与了缺血性脑损伤，采用膜片钳的内面向外式，观察了3min短暂脑缺血后6h、24h以及48h大鼠海马cAl区锥体细胞上BKca通道活动的动态变化，短暂脑缺血后BKca通道的单通道电导和翻转电位均未见明显变化，但通道的开放概率则在缺血预处理后的前24h内显著降低，通道动力学分析显示通道关闭时间变长是短暂脑缺血后通道活动降低的主要原因，因为通道的开放时间未发生明显变化，结果提示短暂脑缺血所致的BKca通道活动降低可能与缺血耐受的产生有关.

为探讨钾通道参与神经元凋亡的可能机制，在星形孢菌素（STS）诱导的培养海马神经元凋亡模型上，研究了凋亡时神经细胞容积的动态变化及钾通道在其中的作用。实验结果显示，钾通道阻断剂四乙铵或升高细胞外K+均能够明显抑制STS诱导的神经元凋亡，并且大电导钙激活钾通道（BK）选择性阻断剂iberiotoxin和paxilline具有同样程度的抗细胞凋亡作用，表明钾通道（可能主要是BK通道）参与了STS诱导的培养海马神经元凋亡，在STS诱导神经元凋亡的早期就出现了细胞容积的显著减少，而钾通道阻断剂或升高细胞外K+均可阻断该细胞容积减少，研究结果提示细胞内钾离子的外流可能参与了凋亡性细胞容积减少，这也可能是钾通道介导细胞凋亡的重要机制之一。

Neurophysiological changes of hippocampal neurons were compared before and after transient forebrain ischemia using intracellu-lar recording and staining techniques in vivo. Ischemic depolarization (ID) was used as an indication of severe ischemia. Under halo-thane anesthesia, approximately 13 rain of ID consistently produced severe neuronal dam-age in the CA1 region of rat hippocampus, while CA3 pyramidal neurons and dentate granule cells remained intact. After such se-vere ischemia, approximately 60% of the CA1 neurons exhibited a synaptic potentia-tion. The excitability of these neurons pro-gressively decreased following reperfusion. Approximately 30% of the CA1 neurons showed a synaptic depression following ischemia. The excitability of these neurons transiently decreased following reperfusion. After ischemia of the same severity, both synaptic transmission and excitability of CA3 and granule cells transiently depressed. These data suggest that ischemia-induced synaptic potentiation may be associated with the pathogenesis of neuronal damage fol-lowing ischemia, and that the synaptic de-pression may have protective effects on hip-pocampal neurons after ischemic insult.

It has been recently reported that potassium channel increases activities in CA1 pyramidal neurons of rat hippocampus following transient forebrain ischemia. To understand the role of the enhanced potassium current in the pathogenesis of neuronal damage after ischemia, we examined the effects of tetraethylammonium (TEA) and 4-aminopyridine (4-AP) on the neuronal injury of CA1 region induced by 15 min forebrain ischemia using a four-vessel occlusion model. Adult rats received intracerebroventricular administration of either TEA or 4-AP after ischemia or TEA before ischemia and once each day for 7 days. In the postischemic TEA treated-rats, the neuronal injury in hippocampal CA1 region was signifi-cantly less than that of the controls. In contrast, neither preischemic infusion of TEA nor postischemic treatment of 4-AP had any neuroprotective effects. The present study demonstrates that postischemic application of TEA protects hippo-campal CA1 pyramidal neurons against ischemic insult, suggesting that potassium channels may play important roles in the pathogenesis of CA1 neuronal death after transient forebrain ischemia.