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首页> 外文期刊>The European Journal of Neuroscience >Dopaminergic control of synaptic plasticity in the dorsal striatum.
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Dopaminergic control of synaptic plasticity in the dorsal striatum.

机译：多巴胺能控制背侧纹状体的突触可塑性。

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摘要

Cortical glutamatergic and nigral dopaminergic afferents impinge on projection spiny neurons of the striatum, providing the most significant inputs to this structure. Isolated activation of glutamate or dopamine (DA) receptors produces short-term effects on striatal neurons, whereas the combined stimulation of both glutamate and DA receptors is able to induce long-lasting modifications of synaptic excitability. Repetitive stimulation of corticostriatal fibres causes a massive release of both glutamate and DA in the striatum and, depending on the glutamate receptor subtype preferentially activated, produces either long-term depression (LTD) or long-term potentiation (LTP) of excitatory synaptic transmission. D1-like and D2-like DA receptors interact synergistically to allow LTD formation, while they operate in opposition during the induction phase of LTP. Corticostriatal synaptic plasticity is severely impaired after chronic DA denervation and requires the stimulation of DARPP-32, a small protein expressed in dopaminoceptive spiny neurons which acts as a potent inhibitor of protein phosphatase-1. In addition, the formation of LTD and LTP requires the activation of PKG and PKA, respectively, in striatal projection neurons. These kinases appear to be stimulated by the activation of D1-like receptors in distinct neuronal populations.
机译：皮质谷氨酸能和黑质多巴胺能传入神经撞击在纹状体的突出棘神经元上，为该结构提供了最重要的输入。谷氨酸或多巴胺（DA）受体的孤立激活对纹状体神经元产生短期影响，而谷氨酸和DA受体的联合刺激能够诱导突触兴奋性的持久改变。皮质皮质纤维的重复刺激导致纹状体中谷氨酸和DA的大量释放，并根据优先激活的谷氨酸受体亚型，产生兴奋性突触传递的长期抑制（LTD）或长期增强（LTP）。 D1样和D2样DA受体协同相互作用，允许LTD形成，而它们在LTP的诱导期相反。慢性DA去神经支配后，皮质口突触可塑性严重受损，需要刺激DARPP-32，DARPP-32是一种在多巴胺感受性多刺神经元中表达的小蛋白，可作为一种有效的蛋白磷酸酶-1抑制剂。此外，LTD和LTP的形成分别需要纹状体投射神经元中PKG和PKA的激活。在不同的神经元群体中，D1样受体的激活似乎刺激了这些激酶。

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