多巴胺与环磷酸腺苷调节的磷蛋白32 kDa控制着纹状体的长时程抑制和长时程增强，这是两种相反形式的突触可塑性。
Dopamine and cAMP-regulated phosphoprotein 32 kDa controls both striatal long-term depression and long-term potentiation, opposing forms of synaptic plasticity.
作者信息
Calabresi P, Gubellini P, Centonze D, Picconi B, Bernardi G, Chergui K, Svenningsson P, Fienberg A A, Greengard P
机构信息
Clinica Neurologica, Dipartimento di Neuroscienze, Università di Tor Vergata, Rome, Italy.
出版信息
J Neurosci. 2000 Nov 15;20(22):8443-51. doi: 10.1523/JNEUROSCI.20-22-08443.2000.
Abstract
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.
摘要
纹状体神经元中D1样多巴胺（DA）受体的刺激激活了一系列复杂的细胞内信号事件，这在运动控制中至关重要。在中等棘状神经元的皮质纹状体突触处，我们提供的证据表明，DA和环磷酸腺苷调节的32 kDa磷蛋白的D1样受体依赖性激活是诱导长期抑郁（LTD）和长期增强（LTP）这两种相反形式的突触可塑性的关键步骤。此外，LTD和LTP的形成分别需要纹状体投射神经元中蛋白激酶G和蛋白激酶A的激活。这些激酶似乎是由不同神经元群体中D1样受体的激活所刺激的。
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