Chase T N, Oh J D
Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD 20892, USA.
Trends Neurosci. 2000 Oct;23(10 Suppl):S86-91. doi: 10.1016/s1471-1931(00)00018-5.
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.
纹状体中等棘状神经元中涉及多巴胺和谷氨酸相互作用的特征性变化，现在似乎是帕金森病（PD）症状产生的原因。激酶和磷酸酶信号之间的平衡会改变谷氨酸受体的磷酸化状态，进而改变其突触强度。棘状神经元NMDA和AMPA受体的敏化会改变皮质谷氨酸能输入到纹状体，并改变纹状体GABA能输出，从而影响运动功能。可以想象，针对PD中发生改变的棘状神经元机制进行药物靶向治疗将提供一种更安全、更有效的疗法。
