Striatal dopamine- and glutamate-mediated dysregulation in experimental parkinsonism

被引：219

作者：

Chase, TN ^{[1
]}

Oh, JD ^{[1
]}

机构：

[1] NINCDS, Expt Therapeut Branch, NIH, Bethesda, MD 20892 USA

来源：

TRENDS IN NEUROSCIENCES | 2000年 / 23卷 / 10期

关键词：

D O I：

10.1016/S1471-1931(00)00018-5

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Characteristic changes involving interactions between dopamine and glutamate in striatal medium spiny neurons now appear to contribute to symptom production in Parkinson's disease (PD). The balance between kinase and phosphatase signaling modifies the phosphorylation state of glutamate receptors and thus their synaptic strength. Sensitization of spiny-neuron NMDA and AMPA receptors alters cortical glutamatergic input to the striatum and modifies striatal GABAergic output, and thus motor function. Conceivably, the pharmacological targeting of spiny-neuron mechanisms modified in PD will provide a safer and more effective therapy.

引用

页码：S86 / S91

页数：6

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