Sastry B R, Goh J W, Pandanaboina M M
Life Sci. 1984 Jan 23;34(4):323-9. doi: 10.1016/0024-3205(84)90619-2.
In transversely sectioned rat hippocampal slices the effects of 2-amino-5-phosphonovalerate (APV), presumably a selective N-methyl-DL-aspartate antagonist, were examined on the development of long-lasting potentiation (LLP) of the CA1 population spike produced by Schaffer collateral tetanization (100 Hz, 1 s). APF (100 nA, 5 min), when applied 150-200 micron away from the CA1 cell bodies (apical dendritic area), had no significant effect if the population spike was evoked at 0.1 Hz, but produced a depression of the population spike if a 100 Hz tetanus was given during its iontophoresis. This depressant effect of APV was counteracted by verapamil (0.33 microM, 3 min) and LLP induced by the 100 Hz tetanus was unmasked. It is suggested that APV does not antagonize LLP, but only masks it by allowing CA++ influx into CA1 neurones that induces a depression. The results also raise doubts as to the selectivity of APV as an amino acid antagonist.
在横切的大鼠海马切片中，研究了2-氨基-5-磷酸戊酸（APV）（可能是一种选择性N-甲基-DL-天冬氨酸拮抗剂）对由Schaffer侧支强直刺激（100Hz，1秒）所产生的CA1群体峰电位的长时程增强（LLP）发展的影响。当在距离CA1细胞体（顶端树突区域）150 - 200微米处施加APV（100纳安，5分钟）时，如果以0.1赫兹诱发群体峰电位，则没有显著影响，但如果在离子导入期间给予100赫兹的强直刺激，则会使群体峰电位降低。APV的这种抑制作用被维拉帕米（0.33微摩尔，3分钟）抵消，并且由100赫兹强直刺激诱导的LLP被揭示出来。这表明APV并不拮抗LLP，而只是通过允许钙离子流入CA1神经元诱导抑制来掩盖它。这些结果也对APV作为氨基酸拮抗剂的选择性提出了疑问。
