Objective To elucidate the inhibitory effects of recombinant Chinese scorpion neurotoxin BmK IM on seizures induced by pentylenetetrazol (PTZ) and the possible mechanism. Methods After purifying recombinant BmK IM from an E. coil cell line, its toxicity (both LDs0 and minimum lethal dose) on rats was determined. BmK IM was then microinjected into the CA3 region of the right hippocampus and its ability to inhibit the effects of an intraperitoneal injection of PTZ was assessed. The effects of BmK IM on the electrophysiological properties of isolated CA3 pyramidal neurons were then studied using whole-cell patch clamp techniques. Results BmK IM can significantly prolong the latent period of epileptic seizures, decrease the degree of seizures, and decrease the frequency of epileptiform discharges induced by PTZ. At the same time, 24h after injection of BmK IM into the hippocampal tissue, BmK IM significantly reduces the concentration of the neurotransmitter glutamate and alleviates PTZ-induced lesions in the hippocampus. Whole-cell patch clamp recordings indicate that BmK IM inhibits INa of rat hippocampal neurons in a dose-dependent manner. BmK IM significantly shifts the activation curve of INa in a positive direction, indicating that BmK IM enhances the threshold potential of INa. Conclusions BmK IM has significant anti-epileptic properties, and may prove useful as a drug in the therapy of epilepsy. The inhibitory effects of BmK IM on seizures caused by pentylenetetrazol might depend on reductions in the release of presynaptic glutamate via the blocking of Na + channels.

Objective To investigate the effects of antisense glutamic acid decarboxylase (GAD67) oligodeoxynucleo-tide (ODN) on behavior, seizure threshold and EEG of hippocampus in the epileptic rats induced by pentylenetetrazol (PTZ). Methods A model of chronic epilepsy in rats was established by PTZ. The inhibition of GAD67 mRNA expression in hippocampus was selectively induced by antisense oligodeoxynucleotide of GAD67. The effect of antisense GAD67 ODN on behavior, seizure threshold and EEG recording of kindled rats was examined. Results Antisense GAD67 ODN could inhibit the expression of GAD67 mRNA and the concentration of GABA. It also could significantly shorten the latencies of seizure and increase the level of seizure and the frequency of epileptiform discharges. Conclusion The gene of GAD67 may be an anti-seizure gene, which might inhibit epileptiform discharge. The treatment of epilepsy by GAD67 gene will have a bright future.

目的观察黄芪抗神经细胞缺氧损伤的作用。方法用氰化钠造成体外培养新生大鼠大脑皮层神经细胞缺氧模型，比较黄芪组和对照组的细胞形态、存活细胞数（四唑盐微量自动比色检测A值）、乳酸脱氢酶（LDH）值和钾离子（K+）流出的变化。结果缺氧48小时后，对照组A值由缺氧前的0.325±0.031降至0.145±0.011，LDH和K+漏出量分别由65.80±2.90 U/L、5.23±0.11mmol/L增至148.80±8.40 U/L、7.31±0.18 mmol/L。而此时黄芪组A值为0.178±0.011、LDH漏出量为127.25±7.84 U/L，K+含量为6.93±0.15mmol/L。与对照组相比，黄芪组受损程度明显减轻。结论黄芪具有一定的抗神经细胞缺氧损伤作用。