腺苷2A受体(A2AR)大量分布于脑基底节区,和多巴胺D2受体(D2R)及亲代谢型谷氨酸受体(mGluR5)形成异聚体,共同调节纹状体突触前后功能。研究显示左旋多巴诱发异动症PD动物模型纹状体A2AR、mGluR5表达增加,而两受体拮抗剂应用可改善异动症PD动物模型异常行为,从而提出A2AR和mGlu5参与了异动症突触可塑性的改变。 Adenosine 2A receptors (A2AR) are abundantly distributed in the basal ganglia and form heterodimers with the dopamine D2 receptor (D2R) and metabotropic glutamate receptors (mGluR5), which together regulate the presynaptic function of the striatum . Studies have shown that levodopa-induced dyskinesia in animal models of striatum A2AR, mGluR5 expression increased, and two receptor antagonist application can improve the abnormal behavior of animal models of dyskinesia, suggesting that A2AR and mGlu5 involved in the dyskinesia synaptic plasticity change.