Cepeda C, Levine M S
Mental Retardation Research Center, University of California at Los Angeles, 90024-1759, USA.
Dev Neurosci. 1998;20(1):1-18. doi: 10.1159/000017294.
This review examines dopamine (DA) and glutamate receptor interactions in the neostriatum (NS) primarily from a neurophysiological perspective. Historically, a clear understanding of the function of DA in the NS has been difficult because it was considered a classical neurotransmitter with either excitatory or inhibitory actions and because many of the data were obtained by use of varying methodologies. When DA is considered a neuromodulator whose role is to alter how NS cells respond to glutamatergic inputs, many of its actions can be accounted for and predicted with great accuracy within a model of receptor subtype. In this model, DA via activation of D1 receptors potentiates responses mediated by activation of N-methyl-D-aspartate (NMDA) receptors. DA via activation of D2 receptors attenuates responses mediated by activation of non-NMDA receptors. Outcomes of combinations of NMDA and D2 and non-NMDA and D1 receptors are not as predictable. The mechanisms underlying the D1-NMDA receptor interactions appear to involve alterations in cell excitability mediated by activation of Ca2+ conductances and/or phosphorylation of NMDA receptors. Less is known about mechanisms underlying the D2-non-NMDA receptor interaction. The functional implications of this model in setting membrane potentials, signal-to-noise ratio, plasticity and excitotoxicity are discussed.
本综述主要从神经生理学角度探讨新纹状体（NS）中多巴胺（DA）与谷氨酸受体的相互作用。从历史上看，要清楚了解NS中DA的功能一直很困难，因为它被视为具有兴奋性或抑制性作用的经典神经递质，而且许多数据是通过使用不同方法获得的。当DA被视为一种神经调质，其作用是改变NS细胞对谷氨酸能输入的反应方式时，在受体亚型模型中，其许多作用都可以得到很好的解释和预测。在这个模型中，DA通过激活D1受体增强由N-甲基-D-天冬氨酸（NMDA）受体激活介导的反应。DA通过激活D2受体减弱由非NMDA受体激活介导的反应。NMDA与D2受体以及非NMDA与D1受体组合的结果则不太可预测。D1-NMDA受体相互作用的潜在机制似乎涉及由Ca2+电导激活和/或NMDA受体磷酸化介导的细胞兴奋性改变。关于D2-非NMDA受体相互作用的潜在机制，人们了解得较少。本文还讨论了该模型在设定膜电位、信噪比、可塑性和兴奋性毒性方面的功能意义。
