目的:观察代谢型谷氨酸受体(mGluRs)激动药3,5-二羟基苯甘氨酸(DHPG)对大鼠海马CAl区穿通通路(PP通路)诱发长时程抑制的作用及机制。方法:制作Wistar大鼠海马组织脑片,分为DHPG组、DHPG+N-甲基-D-天冬氨酸(NMDA)受体拮抗药AP5组和DHPG+双脉冲刺激(PPR)组(n分别为8、9、8),各组加入相应药物及操作后采用电生理记录加药前、后的场电位的标准化后均值。结果:DHPG组、DHPG+AP5组、PPR组加药前、后场电位均值分别为1.0049±0.101、0.7904±0.02197(n=8,t=15,P〈0.01),1.0224±0.0724、0.828±0.01475(n=9,t=15,P〈0.01),0.9525±0.1691、1.0511±0.2934(n=8,t=5,P〈0.01)。结论:DHPG可诱发大鼠海马长时程抑制,且其属于mGluRs依赖型而非NMDA受体依赖型,并通过突触后诱发所致。
OBJECTIVE: To investigate the mechanism of the inductive effect of metabotropic glutamate receptors (GluRs) agonist DHPG on long- term depression in hippocampal CA1 perforant pathway of rats. METHODS: Hippocampal tissue slices of Wistar rats were prepared and divided into three groups: DHPG group (n : 8), DHPG + NMDA receptor antagonist AP5 group (n ~ 9), and DHPG + paired-pulse stimulation (PPR) group (n : 8). The standardized mean values of the field potential before and after drug treatment were recorded with the use of electrophysiological technology. RESULTS: The mean values of the field potential before vs. after drug treatment in the three groups were 1.004 9± 0.101 vs. 0.790 4 ± 0.02197(n=8, t =15, P〈0.01), 1.0224±0.0724vs. 0.828±0.01475(n=9, t :15, P〈0.01), and0.9525±0.1691 vs. 1.051 1± 0.293 4 (n = 8, t= 5, P〈0.01), respectively. CONCLUSION: DHPG can induce hippocampal long - term depression in mGluRs- dependent manner rather than NMDA receptor- dependent manner via a postsynaptic pathway.