哌甲酯、氯安酮长期作用对大鼠海马CA1区突触可塑性的影响  

Chronic Effect of Methylphenidate and Ketamine on Synaptic Plasticity in Rat Hippocampus CA1 Region

作　　者：许崇涛[1] 刘协和 吴前[1] 柴慧霞[1] 

机构地区：[1]汕头大学医学院精神病学教研室,华西医科大学附一院精神科,华西医科大学附一院生理教研室

出　　处：《汕头大学医学院学报》1996年第2期8-11,共4页Journal of Shantou University Medical College

摘　　要：本研究利用离体海马脑片技术，观察多巴胺激动剂哌甲酯和ＮＭＤＡ受体拮抗剂氯安酮（６ｍｇ／ｋｇ）长期肌往后（６周），对大鼠海马ＣＡ１区突触可塑性的影响。结果发现，串刺激（１００个脉冲，１００Ｈｚ）后，氯安酮组大鼠海马脑片ＣＡ１区场兴奋性突触后电位斜率的增高，突触增强的脑片数和长时程增强形成率低于哌甲酯组和对照组，哌甲酯与对照组无差异。提示海马突触可塑性受抑制与ＮＭＤＡ受体功能低下有关，而与多巴胺功能亢进无涉。By using in vitro rat's hippocampal slices, the synaptic plasticity in CA1 of the rats chronically injected (6 weeks, 6mg/kg) with methylphenidate(dopamine agoist) or ketamine (NMDA receptor antagonist) was investigated. The results revealed that in CA1 hippocampus in vitro subjected to the bursts of stimulation(100 pulses at 100 Hz), the augment of the slope of field excitatory postsynaptic potentials(f-EPSPs) was less obvious, while the number of the slices with potentiated f-EPSPs, and the amount of long-term potentiation were smaller in the ketamine group than those in the methylphenidate group and the control group. It can be concluded that the suppression of synaptic plasticity in hippocampus possibly relates to the blockade of the NMDA receptor, but not to the dopamine overactivity.

关 键 词：哌甲酯 氯安酮 突触可塑性 海马脑片 

分 类 号：R338[医药卫生—人体生理学]