Striatal A2A adenosine receptors differentially regulate spontaneous and K+-evoked glutamate release in vivo in young and aged rats
Striatal A2A adenosine receptors differentially regulate spontaneous and K+-evoked glutamate release in vivo in young and aged rats
复制标题
DOI：
10.1097/00001756-199903170-00005
复制
发表时间：
1999-03-17
期刊：
影响因子：
1.7
通讯作者：
Pedata, F
中科院分区：
文献类型：
--
作者：
Corsi, C;Melani, A;Pedata, F
通过微透析实验研究了腺苷 A(2A) 受体激动剂 CGS 21680 对年轻和年老大鼠纹状体谷氨酸和天冬氨酸释放的影响。 CGS 21680 (10 mu M) 显着增加了年轻大鼠的谷氨酸和天冬氨酸自发流出，但在老年大鼠中则不然。相反，CGS 21680 在年轻和老年大鼠中均诱导 K+ 诱发的谷氨酸流出量同样减少。较低剂量的 CGS 21680 (1 μM) 未能改变自发或 K+ 诱发的流出。提示A(2A)激动剂对兴奋性氨基酸流出的相反作用可能分别由位于谷氨酸末端和纹状体间接输出途径上的纹状体A(2A)腺苷受体介导。 NeuroReport 10:687-691 (C) 1999 Lippincott Williams & Wilkins。
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.