AGE-RELATED-CHANGES IN TRANSMITTER GLUTAMATE AND NMDA RECEPTOR CHANNELS IN THE BRAIN OF SENESCENCE-ACCELERATED MOUSE

被引：57

作者：

KITAMURA, Y ^{[1
]}

ZHAO, XH ^{[1
]}

OHNUKI, T ^{[1
]}

TAKEI, M ^{[1
]}

NOMURA, Y ^{[1
]}

机构：

[1] HOKKAIDO UNIV,FAC PHARMACEUT SCI,DEPT PHARMACOL,SAPPORO,HOKKAIDO 060,JAPAN

来源：

NEUROSCIENCE LETTERS | 1992年 / 137卷 / 02期

关键词：

GLUTAMATERGIC NEURON; NMDA RECEPTOR CHANNEL; LEARNING AND MEMORY; AGING; HIPPOCAMPUS; CEREBRAL CORTEX; SENESCENCE-ACCELERATED MOUSE;

D O I：

10.1016/0304-3940(92)90396-O

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The senescence-accelerated mouse (SAM-P/8) is known as a murine model of aging and memory dysfunction. In the hippocampus and cerebral cortex of P/8, the contents of glutamic acid and glutamine were significantly higher than those of normal strain R/1 during 2 and 14 months. High K+-evoked endogenous glutamic acid release from the slices of P/8 was increased in comparison with R/1 at 9 and 11 months. In addition, the B(max) of [H-3]dizocilpine (MK-801, channel blocker for N-methyl-D-aspartic acid receptor/channel) binding in the cerebral cortex was age-dependently decreased in P/8 but not in R/1. These results suggest that synaptic dysfunctions in the glutamatergic system occur in the CNS of SAM-P/8.

引用

页码：169 / 172

页数：4

共 21 条

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