Gołembiowska K, Zylewska A
Department of Pharmacology, Polish Academy of Sciences, Kraków, Poland.
Pol J Pharmacol. 1997 Sep-Oct;49(5):317-22.
The aim of present study was to assess the role of activation of adenosine A-1 and A-2a receptors in the modulation of dopamine (DA) and glutamate release in the rat striatum by microdialysis in freely moving animals. Adenosine A-1 receptor agonist N6-cyclopentyladenosine (CPA) and A-2a receptor agonist 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamidoadenosine (CGS 21680) were administered locally into the striatum through microdialysis probe. CPA (10, 100 and 500 microM) did not affect basal levels of DA or glutamate. In contrast, CGS 21680 at the concentrations of 10, 50 and 100 microM increased in a dose-dependent manner the level of DA and at 100 microM also the level of glutamate. Both agonists at the concentration of 100 microM inhibited KCl-induced (100 mM) DA and glutamate release. The present results suggest, that in physiological conditions only excitatory effects of adenosine may be observed and adenosine A-2a receptors seem to be involved. During depolarization with KCl, adenosine, by inhibiting excessive outflow of neurotransmitters mediated via A-1 and A-2a receptors, manifests its protective role as homeostatic neuromodulator.
本研究的目的是通过在自由活动动物中进行微透析，评估腺苷A-1和A-2a受体激活在调节大鼠纹状体中多巴胺（DA）和谷氨酸释放方面的作用。腺苷A-1受体激动剂N6-环戊基腺苷（CPA）和A-2a受体激动剂2-p-（2-羧乙基）苯乙氨基-5'-N-乙基羧酰胺腺苷（CGS 21680）通过微透析探针局部注入纹状体。CPA（10、100和500微摩尔）不影响DA或谷氨酸的基础水平。相反，10、50和100微摩尔浓度的CGS 21680以剂量依赖性方式增加DA水平，100微摩尔时也增加谷氨酸水平。两种激动剂在100微摩尔浓度时均抑制氯化钾（100毫摩尔）诱导的DA和谷氨酸释放。目前的结果表明，在生理条件下，可能仅观察到腺苷的兴奋作用，且腺苷A-2a受体似乎参与其中。在用氯化钾去极化期间，腺苷通过抑制经由A-1和A-2a受体介导的神经递质过度外流，作为稳态神经调节剂发挥其保护作用。
