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Such epileptoid activities were not influenced by the synaptic receptor inhibitors, and were obviously related to tile persistent sodium current.

这种癫痫样放电的产生不受突触传递阻断剂的影响,但与持续性钠电流明显相关。

These epileptoid bursts were not blocked by a mixture of CNQX, AP-5 and Bic, but by low dose of TTX.

这种放电不被突触阻断剂CNQX+AF-5+Bic阻断,但能被小剂量TTX阻断。

Objective To examine the value of Edaravone in the treatment of vascular dementia through ethologic and pathologic changes induced by chronic cerebral ischemiaMethods Wistar rats were randomly divided into sham operated group,model group,edaravone group and duxil groupThe chronic cerebral hypoperfusion models were made by permanent bilateral occlusion of both common carotid arteriesThe memory ability and ultramicrostructure of brain tissue were observedResults The escape latencies in model group were more significantly prolonged than that in the other groups (P<005)But there was no significant difference between edaravone and duxil groupAnd pathologic changes observed by electron microscope in nerve cell of edaravone group and duxil group and model group were fairly light than that in sham operated groupEdaravone group had increased mitochondrium and frontal membranous synaptic vesicle and more productive metabolic activityConclusions Edaravone can lessen injures of hippocampal neurons loss to improve the spatial learning and memory abilitiesAnd it is proved further that edaravone can treat VD

目的 观察依达拉奉对慢性缺血致血管性痴呆大鼠行为学及形态学的影响,探讨依达拉奉在治疗VD中的应用价值。方法实验分假手术组、模型组及都可喜对照组及依达拉奉治疗组,应用双侧颈总动脉结扎方法制备慢性脑缺血大鼠痴呆模型,观察各组大鼠的记忆功能及脑组织超微结构改变。结果缺血组水迷宫表现同对照组、都可喜组及依达拉奉组相比有显著差异(P<005),依达拉奉组与都可喜组相比未见显著差异。同时电镜观察结果也发现依达拉奉组及都可喜组与模型组及假手术组相比神经细胞病理改变较轻,且依达拉奉组线粒体及前膜突触小泡增多,代谢活动较都可喜组旺盛。结论依达拉奉可能通过减轻海马神经元的损伤来改善慢性脑缺血大鼠空间学习记忆障碍,证明依达拉奉对慢性缺血致VD大鼠具有治疗作用。

Calcium/calmodulin- dependent protein kinase II was proposed to play a prominent role in regulation of excitatory synaptic transmission.

Ca2+/钙调蛋白依赖的蛋白激酶II在兴奋性突触传递的调节过程中发挥着重要作用。

GABA is resitent to the toxicity of the excitory amino acids because it can promote the conduct of Cl-, prevent the depolarization of the postsynaptic inhibition effectively and the open of Ca2+-gated channel, reduce the metabolic rate of the ischemic nurons.

GABA可以拮抗兴奋性氨基酸的毒性作用,它主要通过促进氯离子的传导,有效的阻断突触后去极化及电压依赖性Ca2+通道的开放,降低正常灌注/缺血性神经元的代谢率和氧的消耗,从而使神经元易耐受缺血性损伤[9]。

Gliosis plays a critical role in post-traumatic epileptogenesis. The inhibition of the proliferation of astrocytes with 7β OHCH could influence synaptic plasticity, modulate the imbalance of excitatory and inhibitory systems in hippocampus and postpone the latency between injury and the occurrence of chronic spontaneous seizures, furthermore to some extent, reduce the occurrence of post-traumatic epilepsy.

星形胶质细胞增生在创伤性癫痫发病机制中起重要作用,抑制胶质细胞增生,可影响海马突触可塑性,有利于调整海马内兴奋性和抑制性功能系统之间作用的失衡,可延长损伤与发生慢性自发性抽搐之间的间歇期,在一定程度上降低创伤性癫痫的发病率。

In this research, based on setting up the rat model of ischemic apoplexy successfully, we demonstrated there was down-regulation cerebral zone in its brain, which was manifested by hypoperfusion in the maginal and remote zone to infact area, hypoactivity of synapses and cerebral capillary endothelial cell to modulate microvascular.

本课题成功制作了缺血性卒中后遗症大鼠模型,并证实了下调脑区的存在,即梗死灶边缘区及远隔区存在低灌注现象,突触活性降低,脑微血管内皮细胞对脑微循环的调节机能下降。

Dementia and cognitive impairments in Alzheimer's disease have been attributed to hypofunction of cholinergic system in the brain.

阿尔采默病导致的痴呆和认知障碍等症状,主要是由于脑内胆碱能突触传递受损引起的。

Under these two kinds of stimuli, thalamocortical pathway shows prominent properties of short-term synaptic depression, which is alike those of intracortical synapses.

在这两种刺激模式下,正常成年大鼠的丘脑皮层主要视觉通路均表现出明显的短时程抑制特性,并且与皮层内突触的特性相似。

NOS neurons atrophy markedly in laterodorsal tegmental nucleus of aged mice. NOS neurons and synapses atrophy in Alzheimer's disease patient temporal cortex and amygdala, NOS neurons decrease by 18-33% in hippocampus.

衰老时NOS神经元发生了某些变化,老龄小鼠被盖背外侧核NOS神经元明显萎缩;Alzheimer's病人颞叶皮层和杏仁核NOS细胞及突触显著绉缩,海马分子层内侧1/3缺少NOS神经元,NOS神经元减少18~30%。

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She gently rebuff ed him, but agreed that they could be friends

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