Striatal A2A adenosine receptors differentially regulate spontaneous and K+-evoked glutamate release in vivo in young and aged rats

被引：61

作者：

Corsi, C ^{[1
]}

Melani, A ^{[1
]}

Bianchi, L ^{[1
]}

Pepeu, G ^{[1
]}

Pedata, F ^{[1
]}

机构：

[1] Univ Florence, Dept Preclin & Clin Pharmacol, I-50139 Florence, Italy

来源：

NEUROREPORT | 1999年 / 10卷 / 04期

关键词：

A(2A) adenosine receptor; ageing; aspartate; glutamate; microdialysis; striatum;

D O I：

10.1097/00001756-199903170-00005

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

THE effect of the adenosine A(2A) receptor agonist CGS 21680 on glutamate and aspartate release was investigated in the striatum of young and old rats by microdialysis experiments. CGS 21680 (10 mu M) significantly increased glutamate and aspartate spontaneous outflow in young-but not in old rats. On the contrary, CGS 21680 induced the same decrease in K+-evoked glutamate outflow in both young and aged rats. A lower dose of CGS 21680 (1 mu M) failed to modify either spontaneous or K+-evoked outflow. It is suggested that the opposite effects of the A(2A) agonist on excitatory amino acid outflow may be respectively mediated by striatal A(2A) adenosine receptors located on glutamatergic terminals and on the striatal indirect output pathway. NeuroReport 10:687-691 (C) 1999 Lippincott Williams & Wilkins.

引用

页码：687 / 691

页数：5

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