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中国临床药理学与治疗学 ›› 2007, Vol. 12 ›› Issue (11): 1264-1268.

• 基础研究 • 上一篇    下一篇

丙泊酚对大鼠海马CA1 区长时程增强的影响

魏辉明, 杨云丽, 麻伟青, 于涛, 李治贵, 李文锋   

  1. 成都军区昆明总医院麻醉科, 昆明650032, 云南
  • 收稿日期:2007-08-12 修回日期:2007-09-13 发布日期:2020-11-04
  • 作者简介:魏辉明, 男, 博士, 副主任医师, 研究方向:麻醉及疼痛临床药理学。Tel:0871-4774724 E-mail: medicana@sina.com

Effects of propofol on long-term potentiation of CA1 area in rat hippocampus in vivo

WEI Hui-ming, YANG Yun-li, MA Wei-qing, YU Tao, LI Zhi-gui, LI Wen-feng   

  1. Department of Anesthesiology, Kunming General Hospital of Chengdu Military Area, Kunming 650032,Yunnan, China
  • Received:2007-08-12 Revised:2007-09-13 Published:2020-11-04

摘要: 目的: 研究丙泊酚对大鼠海马CA1 区长时程增强(LTP) 表达的影响, 并探讨其机制。方法: 63 只戊巴比妥钠麻醉大鼠分多组, 分别观察腹腔注射丙泊酚20 mg/kg 对海马CA1 区树突层兴奋性突触后膜电位(EPSP)、LTP 表达的影响以及与D-2-氨基-5-磷酸戊酸(APV) 和6-氰基-7-硝基喹啉-2, 3-二酮(CNQX) 合用时对LTP 表达的影响。结果: 各组基础EPSP 幅值稳定;高频刺激(HFS) 前应用丙泊酚引出的LTP 与对照组相当(P>0.05),HFS 后LTP 幅值明显低于对照组(P<0.01); 丙泊酚合用APV 后不能引出LTP, 合用CNQX 后幅值一过性升高后, 迅速下降并低于基线(P<0.05) 。结论: 丙泊酚20 mg/kg 腹腔注射不影响戊巴比妥钠麻醉大鼠海马CA1 区N-甲基-D-门冬氨酸(NMDA) 受体依赖型LTP诱导, 但可影响其维持;其机制与阻滞α-氨基-3-羟基-5-甲基恶唑-4-丙酸(AMPA) 受体有关, 与NMDA受体功能状态无关。

关键词: 丙泊酚, 长时程增强, 兴奋性突触后膜电位, 受体, 大鼠海马

Abstract: AIM: To study the effects of propofol on long-term potentiation (LTP) in the CA1 area of rat hippocampus in vivo and to elucidate the possible underlying mechanisms. METHODS: 63 pentobarbitone-anaesthetized rats were used to investigate the effects of propofol (20 mg/kg, i. p.) alone and with NMDA or AMPA receptor antagonists (APV or CNQX) on excitatory postsynaptic potential (EPSP) and LTP expression of the CA1 stratum radiatum of the rat hippocampus by using stereotaxic technology and extracellular recording. RESULTS: Baseline EPSP amplitudes of all groups were stable. During treatment with propofol before high f requency stimulation (HFS),LTP amplitude was the same as that of control (P>0.05),whereas when given after HFS, propofol significantly lowered the amplitude of LTP compared with control (P<0.01). On the other hand, LTP could not be induced after treatment of propofol with APV, however, the amplitude of LTP increased transiently and decreased to baseline rapidly after treatment with propofol and CNQX (P<0.05). CONCLUSION: Propofol did not affect the induction of LTP which is dependent on NMDA receptors in the CA1 area of the rat hippocampus but propofol did inhibit the LTP maintenance, which may be attributed to blockade of AMPA receptors but not to NMDA receptors.

Key words: propofol, long-term potentiation, excitatory post-synaptic potential, receptor, rat, hippocampus

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