Tang K, Low M J, Grandy D K, Lovinger D M
Department of Molecular Physiology and Biophysics and Center for Molecular Neuroscience, Vanderbilt University Medical School, Nashville, TN 37232-0615, USA.
Proc Natl Acad Sci U S A. 2001 Jan 30;98(3):1255-60. doi: 10.1073/pnas.98.3.1255. Epub 2001 Jan 16.
The neurotransmitters dopamine (DA) and glutamate in the striatum play key roles in movement and cognition, and they are implicated in disorders of the basal ganglia such as Parkinson's disease. Excitatory synapses in striatum undergo a form of developmental plasticity characterized by a decrease in glutamate release probability. Here we demonstrate that this form of synaptic plasticity is DA and DA D2 receptor dependent. Analysis of spontaneous synaptic responses indicates that a presynaptic mechanism involving inhibition of neurotransmitter release underlies the developmental plasticity. We suggest that a major role of DA in the striatum is to initiate mechanisms that regulate the efficacy of excitatory striatal synapses, producing a decrease in glutamate release.
纹状体中的神经递质多巴胺(DA)和谷氨酸在运动和认知中发挥关键作用,并且它们与帕金森病等基底神经节疾病有关。纹状体中的兴奋性突触经历一种发育可塑性形式,其特征是谷氨酸释放概率降低。在这里,我们证明这种形式的突触可塑性依赖于多巴胺和多巴胺D2受体。对自发突触反应的分析表明,一种涉及抑制神经递质释放的突触前机制是发育可塑性的基础。我们认为,多巴胺在纹状体中的一个主要作用是启动调节兴奋性纹状体突触效能的机制,导致谷氨酸释放减少。