Harris E W, Stevens D R, Cotman C W
Department of Psychobiology, University of California Irvine 92717.
Brain Res. 1987 Aug 25;418(2):361-5. doi: 10.1016/0006-8993(87)90104-1.
The glutamate analog 2-amino-4-phosphonobutyrate (AP4), which in control slices has little effect on Schaffer synaptic responses in hippocampal area CA1, reduces Schaffer responses in slices treated with quisqualate. We have shown that this effect of AP4 is associated with depolarization of CA1 neurons and a persisting small reduction in Schaffer response amplitude. 2-Amino-6-phosphonohexanoate also depressed Schaffer responses following priming with quisqualate, but 2-amino-7-phosphonoheptanoate did not. Treatment with alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) or N-methyl-D-aspartate (NMDA) did not sensitize slices to AP4. The pharmacology of this 'priming effect' of quisqualate corresponds to that of a putative uptake site. We suggest the effects of AP4 (and AP6) result from exchange for previously accumulated quisqualate.
谷氨酸类似物2-氨基-4-膦酰丁酸（AP4），在对照切片中对海马CA1区的沙弗尔突触反应影响很小，但在用喹啉酸处理的切片中会降低沙弗尔反应。我们已经表明，AP4的这种作用与CA1神经元的去极化以及沙弗尔反应幅度持续小幅降低有关。2-氨基-6-膦酰己酸在用喹啉酸引发后也会抑制沙弗尔反应，但2-氨基-7-膦酰庚酸则不会。用α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）或N-甲基-D-天冬氨酸（NMDA）处理不会使切片对AP4敏感。喹啉酸这种“引发效应”的药理学与一个假定的摄取位点相符。我们认为AP4（和AP6）的作用是由于与先前积累的喹啉酸进行交换所致。
