Kubo T, Kohira R, Okano T, Ishikawa K
Department of Pharmacology, Nihon University School of Medicine, Tokyo, Japan.
Brain Res. 1993 Jul 9;616(1-2):311-4. doi: 10.1016/0006-8993(93)90223-a.
Neonatal Wistar rats were subcutaneously injected with 0.1, 1, or 2 mg/g b.wt. of monosodium glutamate (MSG) at 1, 3, 5, 7, and 9 days after birth. The animals were observed for degeneration of pyramidal cells in the hippocampus. The histological change disappeared when the animals were concurrently injected with glutamate diethyl ester (GDEE), an antagonist of the glutamate receptor. When light-dark discrimination learning was carried out at 10 weeks old, the correct response in the acquisition period was impaired in the animals given 1 and 2 mg/g of neonatal MSG. Their retention scores were also impaired in comparison with the control animal. The behavioral impairment recovered with pre-treatment with GDEE. No significant changes were observed in the concentrations of transmitter substances, including amino acids and monoamines. These results suggest that neonatal MSG destroys the hippocampus and impairs acquisition and retention of discrimination learning through the mechanism of glutamate receptors.
新生Wistar大鼠在出生后1、3、5、7和9天皮下注射0.1、1或2mg/g体重的味精（MSG）。观察动物海马中锥体细胞的退化情况。当动物同时注射谷氨酸二乙酯（GDEE，一种谷氨酸受体拮抗剂）时，组织学变化消失。在10周龄时进行明暗辨别学习，给予1和2mg/g新生期味精的动物在习得期的正确反应受损。与对照动物相比，它们的记忆分数也受损。经GDEE预处理后，行为障碍得以恢复。在包括氨基酸和单胺在内的递质物质浓度方面未观察到显著变化。这些结果表明，新生期味精通过谷氨酸受体机制破坏海马，并损害辨别学习的习得和记忆。
