Izumi Y, Zorumski C F
Department of Psychiatry, Washington University School of Medicine, St. Louis, MO 63110.
Neuroreport. 1993 Sep;4(9):1131-4.
Stimulation of the Schaffer collateral projection to the CA1 region in rat hippocampal slices at 1 Hz for 15 min produced a N-methyl-D-aspartate (NMDA) receptor-dependent long-term depression (LTD) of synaptic responses and, when given after tetanic stimulation, reversed long-term potentiation (LTP). Both LTD and the reversal of LTP were blocked by the nitric oxide (NO) inhibitor L-NG-monomethylargine (L-NMMA). L-NG-nitroarginine (L-NOArg) and hemoglobin also blocked LTD. The inhibition of LTD by L-NMMA was overcome by L- but not D-arginine. Sodium nitroprusside and S-nitrosocysteine, agents that spontaneously release NO, mimicked the effect of 1 Hz stimulation. These results indicate that NO mediates LTD produced by sustained 1 Hz activation of CA1 synapses and support the hypothesis that NO mediates the inhibition of LTP produced by untimely activation of NMDA receptors.
以1赫兹的频率刺激大鼠海马切片中向CA1区投射的Schaffer侧支15分钟，会产生一种依赖于N-甲基-D-天冬氨酸（NMDA）受体的突触反应长期抑制（LTD），并且在强直刺激后给予时，会逆转长期增强（LTP）。LTD和LTP的逆转均被一氧化氮（NO）抑制剂L-NG-单甲基精氨酸（L-NMMA）阻断。L-NG-硝基精氨酸（L-NOArg）和血红蛋白也阻断LTD。L-NMMA对LTD的抑制作用可被L-精氨酸而非D-精氨酸克服。硝普钠和S-亚硝基半胱氨酸这两种能自发释放NO的物质，模拟了1赫兹刺激的效果。这些结果表明，NO介导了由CA1突触持续1赫兹激活所产生的LTD，并支持了NO介导由NMDA受体过早激活所产生的LTP抑制作用这一假说。
