Stone T W
Department of Physiology, St George's Hospital Medical School, University of London, U.K.
Neurosci Lett. 1988 Jan 22;84(2):234-8. doi: 10.1016/0304-3940(88)90414-4.
The N-methyl-D-aspartate (NMDA) receptor blocker 2-amino-5-phosphonovaleric acid [+/-)-2-APV) and kynurenic acid both suppressed spontaneous epileptiform burst discharges in the CA3 region of rat hippocampal slices. When the bursts were induced by perfusion with magnesium-free medium (+/-)-2-APV was the more potent inhibitor (ED50 66 microM for (+/-)-2-APV and 110 microM for kynurenate). When bursts were induced by picrotoxin, kynurenate was more potent with an ED50 of 132 microM, compared with 290 microM for (+/-)-2-APV. Both antagonists were selective inhibitors of responses to NMDA when examined against excitations induced by NMDA, kainate and quisqualate applied by microiontophoresis onto CA3 pyramidal cells. The results may indicate a complex receptor profile for endogenous compounds involved in epileptiform bursts, or the existence of non-pyramidal cells bearing non-NMDA receptors sensitive to kynurenic acid.
N-甲基-D-天冬氨酸（NMDA）受体阻断剂2-氨基-5-磷酸基戊酸[（±）-2-APV]和犬尿喹啉酸均能抑制大鼠海马脑片CA3区的自发性癫痫样爆发放电。当通过灌注无镁培养基诱导爆发时，（±）-2-APV是更有效的抑制剂（（±）-2-APV的半数有效剂量（ED50）为66微摩尔，犬尿酸盐为110微摩尔）。当通过苦味毒诱导爆发时，犬尿酸盐更有效，ED50为132微摩尔，而（±）-2-APV为290微摩尔。当针对通过微量离子电泳施加到CA3锥体细胞上的NMDA、海人藻酸和quisqualate诱导的兴奋进行检测时，这两种拮抗剂都是对NMDA反应的选择性抑制剂。结果可能表明参与癫痫样爆发的内源性化合物具有复杂的受体谱，或者存在对犬尿喹啉酸敏感的非NMDA受体的非锥体细胞。
