Dopamine and cAMP-regulated phosphoprotein 32 kDa controls both striatal long-term depression and long-term potentiation, opposing forms of synaptic plasticity
Dopamine and cAMP-regulated phosphoprotein 32 kDa controls both striatal long-term depression and long-term potentiation, opposing forms of synaptic plasticity
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DOI：
10.1523/jneurosci.20-22-08443.2000
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发表时间：
2000-11-15
影响因子：
5.3
通讯作者：
Greengard, P
中科院分区：
文献类型：
--
作者：
Calabresi, P;Gubellini, P;Greengard, P
在运动控制中至关重要的一系列复杂的细胞内信号事件通过刺激纹状体神经元中的D1样多巴胺（DA）受体而激活。在中等多刺神经元的皮质纹状体突触中，我们提供的证据表明，DA和环腺苷3 '，5'单磷酸调节的磷蛋白32 kDa的D1样受体依赖性激活是诱导长时程抑制（LTD）和长时程增强（LTP）的关键步骤，这两种相反形式的突触可塑性。此外，LTD和LTP的形成需要激活蛋白激酶G和蛋白激酶A，分别在纹状体投射神经元。这些激酶似乎是由不同的神经元群体中的D1样受体的激活所刺激的。
A complex chain of intracellular signaling events, critically important in motor control, is activated by the stimulation of D1-like dopamine (DA) receptors in striatal neurons. At corticostriatal synapses on medium spiny neurons, we provide evidence that the D1-like receptor-dependent activation of DA and cyclic adenosine 3',5' monophosphate-regulated phosphoprotein 32 kDa is a crucial step for the induction of both long-term depression (LTD) and long-term potentiation (LTP), two opposing forms of synaptic plasticity. In addition, formation of LTD and LTP requires the activation of protein kinase G and protein kinase A, respectively, in striatal projection neurons. These kinases appear to be stimulated by the activation of D1-like receptors in distinct neuronal populations.