腺苷 A2A 受体的阻断可防止皮质刺激诱导的纹状体蛋白磷酸化。
Blockade of adenosine A2A receptors prevents protein phosphorylation in the striatum induced by cortical stimulation.
作者信息
Quiroz César, Gomes Catarina, Pak Arlene C, Ribeiro Joaquim A, Goldberg Steven R, Hope Bruce T, Ferré Sergi
机构信息
Behavioral Neuroscience Branch, National Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, Department of Health and Human Services, Baltimore, Maryland 21224, USA.
出版信息
J Neurosci. 2006 Oct 18;26(42):10808-12. doi: 10.1523/JNEUROSCI.1661-06.2006.
Abstract
Previous studies have shown that cortical stimulation selectively activates extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation and immediate early gene expression in striatal GABAergic enkephalinergic neurons. In the present study, we demonstrate that blockade of adenosine A2A receptors with caffeine or a selective A2A receptor antagonist counteracts the striatal activation of cAMP-protein kinase A cascade (phosphorylation of the Ser845 residue of the glutamate receptor 1 subunit of the AMPA receptor) and mitogen-activated protein kinase (ERK1/2 phosphorylation) induced by the in vivo stimulation of corticostriatal afferents. The results indicate that A2A receptors strongly modulate the efficacy of glutamatergic synapses on striatal enkephalinergic neurons.
摘要
先前的研究表明，皮质刺激可选择性激活纹状体γ-氨基丁酸能脑啡肽能神经元中的细胞外信号调节激酶1/2（ERK1/2）磷酸化和即刻早期基因表达。在本研究中，我们证明用咖啡因或选择性A2A受体拮抗剂阻断腺苷A2A受体会抵消体内皮质纹状体传入纤维刺激所诱导的纹状体中环磷酸腺苷-蛋白激酶A级联反应（α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体谷氨酸受体1亚基的Ser845残基磷酸化）和丝裂原活化蛋白激酶（ERK1/2磷酸化）的激活。结果表明，A2A受体强烈调节谷氨酸能突触对纹状体脑啡肽能神经元的作用效果。
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