Hösli L, Hösli E, Lehmann R, Eng P
Neurosci Lett. 1983 Mar 28;36(1):59-62. doi: 10.1016/0304-3940(83)90486-x.
Glutamate and the glutamate analogue AMPA ((RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid) caused depolarizations of cultured rat spinal and brainstem neurones which were reversibly antagonized by the glutamate antagonist glutamic acid diethylester (GDEE) but not by 2-amino-5-phosphonovalerate (APV), an N-methyl-D-aspartate (NMDA) antagonist. In contrast, depolarizations by NMDA were blocked by APV but not by GDEE. These results suggest that the depolarization by AMPA is caused by the activation of glutamate/quisqualate-preferring receptors.
谷氨酸和谷氨酸类似物AMPA（（RS）-α-氨基-3-羟基-5-甲基-4-异恶唑丙酸）可使培养的大鼠脊髓和脑干神经元发生去极化，该去极化可被谷氨酸拮抗剂二乙谷氨酸酯（GDEE）可逆性拮抗，但不能被N-甲基-D-天冬氨酸（NMDA）拮抗剂2-氨基-5-磷酸戊酸（APV）拮抗。相反，NMDA引起的去极化可被APV阻断，但不能被GDEE阻断。这些结果表明，AMPA引起的去极化是由谷氨酸/quisqualate偏好性受体的激活所致。
