中文摘要：

为了解静脉全麻药异丙酚对视上核神经元兴奋性突触传递的作用并分析其可能机制，本研究采用细胞内记录技术，观察异丙酚（0．1～3．0mmol／L）对下丘脑冠状切片视上核（supraopticnucleus，SON）神经元突触后电位（postsynapticpotential，PSP）的作用。结果显示，在局部电刺激SON背外侧区域可诱发PSP的8个细胞中，异丙酚能浓度依赖性降低88％细胞的PSP幅度（P〈0．01）、曲线下面积、时程、半幅时程和10％～90％衰减时间俨〈0．05）。1．0mmoUL异丙酚能可逆地完全取消29％（2／7）细胞的PSP。压力喷射外源性谷氨酸在SON神经元诱发伴有膜电阻减小的去极化反应，异丙酚对谷氨酸反应呈可逆的浓度依赖性抑制，但0-3mmol／L异丙酚仅完全取消同步记录的PSP，却未能完全抑制谷氨酸反应。用GABA。受体阻断剂印防己毒素（30mol／L）预处理后，7个细胞兴奋性突触后电位（excitatorypostsynapticpotential，EPSP）增大，再灌流异丙酚后观察到异丙酚对EPSP的抑制作用减弱。结果提示，异丙酚抑NSON神经元兴奋性突触传递的作用可能同时涉及突触前和突触后机制。在突触后可能通过激活GABA。受体而抑制SON神经元的兴奋性突触传递，但高浓度的异丙酚也可能涉及对兴奋性谷氨酸受体的直接抑制。

英文摘要：

The present study was designed to investigate the inhibitory effects of intravenous general anesthetic propofol （0.1-3.0 mmol/L） on excitatory synaptic transmission in supraoptic nucleus （SON） neurons of rats, and to explore the underlying mechanisms by using intracellular recording technique and hypothalamic slice preparation. It was observed that stimulation of the dorsolateral region of SON could elicit the postsynaptic potentials （PSPs） in SON neurons. Of the 8 tested SON neurons, the PSPs of 7 （88%, 7/8） neurons were decreased by propofol in a concentration-dependent manner, in terms of the PSPs＇ amplitude （P 〈 0.01）, area under curve, duration, half-width and 10%-90% decay time （P 〈 0.05）. The PSPs were completely and reversibly abolished by 1.0 mmol/L propofol at 2 out of 7 tested cells. The depolarization responses induced by pressure ejection of exogenous glutamate were reversibly and concentration-dependently decreased by bath application of propofol. The PSPs and glutamate-induced responses recorded simul- taneously were reversibly and concentration-dependently decreased by propofol, but 0.3 mmol/L propofol only abolished PSPs. The excitatory postsynaptic potentials （EPSPs） of 7 cells increased in the condition of picrotoxin （30 9mol/L, a GABAA receptor antago- nist） pretreatment. On this basis, the inhibitory effects of propofol on EPSPs were decreased. These data indicate that the presynaptic and postsynaptic mechanisms may be both involved in the inhibitory effects of propofol on excitatory synaptic transmission in SON neurons. The inhibitory effects of propofol on excitatory synaptic transmission of SON neurons may be related to the activation of GABAA receptors, but at a high concentration, propofol may also act directly on glutamate receptors.