摘要
目的:探讨单唾液酸神经节苷脂(monosialotetrahexosylganglioside,GM1)对大鼠短暂脑缺血后海马CA1区突触传递长时程增强(long-termpo-tentiation,LTP)效应的保护作用。方法:采用短暂夹闭双侧颈总动脉30min复制大鼠脑缺血模型。1周后通过在体记录观察其海马CA1区LTP的变化,以及缺血后给予GM1的干预作用。结果:强直刺激可以诱导多数大鼠的海马CA1区锥体细胞产生LTP,表现为群体峰电位(popularspika,PS)振幅及群体兴奋性突触后电位(fieldexcitedpostsynapticpotential,fEPSP)斜率明显升高,并持续30min以上。但缺血组LTP的PS振幅和fEPSP变化率犤(21.4±4.3)%犦LTP效应强度均明显低于对照组犤(70.2±9.7)%犦,表现为LTP诱导障碍。在GM1治疗组,这种障碍均得到一定程度的缓解,10mg/kgGM1缓解效果犤(71.3±10.8)%犦明显强于5mg/kgGM1犤(46.1±7.8)%犦。结论:缺血后给予GM1可明显提高大鼠短暂脑缺血后海马CA1区强直性LTP的效应强度,改善脑缺血后海马LTP异常,该作用可能为其治疗缺血性脑损伤后学习记忆行为障碍的机制之一。
AIM:To study the protective effects of monosialotetrahexosylganglioside(GM1) on the induction of long-term potentiation(LTP) of synaptic transmission in hippocampal CA1 region of rats after transient cerebral ischemia.METHODS:Cerebral ischemia models of rats were made by transient blocking the common carotid arteries bilaterally for 30 min.The changes of the hippocampal CA1 LTP and the treatment effects of GM1 administrated immediately following ischemia were observed by extracellular recording one week after cerebral ischemia.RESULTS:In most of the normal rats, tetanic stimulation could evoke LTP,which was represented by the significant increase in amplitude of popular spike(PS) and slope of field excited postsynaptic potential(fEPSP),and this change lasted for at least 30 min in the CA1 hippocampal pyramid cells.But in the ischemia group,the amplitude of PS and the slope of fEPSP(LTP intensity)[(21.4±4.3)%] were significantly lower than those in the control group[(70.2±9.7)%].It represented the impediment of LTP induction.In the group of GM1 treatment,this abnormity of LTP induction was partially ameliorated in some extent,and the treatment effect of GM1 at a dosage of 10 mg/kg[(71.3±10.8)%] was much better than that of 5 mg/kg[(46.1±7.8)%].CONCLUSION:Administration of GM1 after ischemia can evidently raise the intensity of tetanic-dependent LTP in the hippocampal CA1 region of rats with transient brain ischemia and ameliorate the abnormity of hippocampal LTP after cerebral ischemia.This may be one of the mechanisms of the effects of GM1 on learning and memory disorders after ischemic brain injury.
出处
《中国临床康复》
CSCD
2004年第7期1278-1279,共2页
Chinese Journal of Clinical Rehabilitation
