Sil'kis I G
Institute of Higher Nervous Activity and Neurophysiology of the Russian Acad. Sci., Russia, 117865, Moscow, Butlerov St., 5a.
Ross Fiziol Zh Im I M Sechenova. 2001 Feb;87(2):155-69.
On the basis of earlier suggested unitary mechanism of synaptic plasticity opposite effects of adenosine and dopamine on the cAMP concentration in striatal spinal cells can emphasize the well known antagonistic interactions between A2A and D2 receptors on striatopallidal cells and between A1 and D1 receptors on striatonigral cells. This is due to that both the dopamine agonist and adenosine antagonist must promote the induction of long-term potentiation/depression of efficacy of excitatory cortical inputs to striatopallidal/striatonigral cells. This modification must lead to synergistic disinhibition of thalamic cells via "direct" and "indirect" pathways through basal ganglia and subsequent strengthening of motor activity.
基于早期提出的突触可塑性单一机制，腺苷和多巴胺对纹状体脊髓细胞中环磷酸腺苷（cAMP）浓度的相反作用，可突出纹状体苍白球细胞上A2A和D2受体之间以及纹状体黑质细胞上A1和D1受体之间众所周知的拮抗相互作用。这是因为多巴胺激动剂和腺苷拮抗剂都必须促进对纹状体苍白球/纹状体黑质细胞兴奋性皮质输入的长期增强/抑制的诱导。这种修饰必须通过基底神经节的“直接”和“间接”途径导致丘脑细胞的协同去抑制，并随后增强运动活动。
