Dopaminergic modulation of short-term synaptic plasticity in fast-spiking interneurons of primate dorsolateral prefrontal cortex
Dopaminergic modulation of short-term synaptic plasticity in fast-spiking interneurons of primate dorsolateral prefrontal cortex
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DOI：
10.1152/jn.00698.2005
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发表时间：
2005-12-01
影响因子：
2.5
通讯作者：
Barrionuevo, G
中科院分区：
文献类型：
--
作者：
Gonzalez-Burgos, G;Kroener, S;Barrionuevo, G
首页--期刊主要分类--期刊细介绍--期刊题录与文摘--期刊详细文摘内容多巴胺能对灵长类背外侧前额叶皮质快峰中间神经元短时突触可塑性的调节。神经生理学杂志94：4168-4177,2005。2005年9月7日首次出版；DOI：10.1152/jn。00698.2005。多巴胺能调节灵长类背外侧前额叶皮质(PFC)的活动对工作记忆等认知功能是必不可少的。然而，PFC中多巴胺神经调节的细胞机制还不是很清楚。我们研究了持续刺激兴奋性输入时，多巴胺受体激活对猴PFC中快速放电的GABA能中间神经元的影响。20 Hz刺激可引起兴奋性突触后电位(EPSP)的短期抑制。D1受体激动剂SKF81297(5 MU M)显著降低了EPSP序列的第一个EPSP的波幅，但不降低其后续反应的波幅，但仍表现出明显的抑制。多巴胺(DA)的作用与SKF81297相似，但可被D_1受体拮抗剂SCH23390(5µM)所阻断，表明该作用是由D_1受体介导的。DA不改变微小的兴奋性突触后电流，提示其作用依赖于活动和突触前动作电位。与前人在锥体神经元中的研究结果不同，在快峰细胞中，N-甲基-D-天冬氨酸受体在阈值下对EPSP的贡献并不显著，并且快峰细胞去极化缩短了EPSP的时程。此外，DA对时间总和没有显著影响。每10列S发出的第一个EPSP波幅的选择性降低表明，在快峰神经元中，DA降低了低频诱发的EPSP的波幅，但不降低重复刺激诱发的EPSP的波幅。因此，DA可以改善对背景突触活动之上的EPSP爆发的检测。表现为短期抑郁的EPSP爆发可能传递突触前棘波序列中包含的依赖于棘波时序的时序代码。因此，DA神经调节可能会增加快峰细胞输入时的信噪比。
Gonzalez-Burgos, G., S. Kroener, J. K. Seamans, D. A. Lewis, and G. Barrionuevo. Dopaminergic modulation of short-term synaptic plasticity in fast-spiking interneurons of primate dorsolateral prefrontal cortex. J Neurophysiol 94: 4168-4177, 2005. First published September 7, 2005; doi: 10.1152/jn. 00698.2005. Dopaminergic regulation of primate dorsolateral prefrontal cortex (PFC) activity is essential for cognitive functions such as working memory. However, the cellular mechanisms of dopamine neuromodulation in PFC are not well understood. We have studied the effects of dopamine receptor activation during persistent stimulation of excitatory inputs onto fast-spiking GABAergic interneurons in monkey PFC. Stimulation at 20 Hz induced short-term excitatory postsynaptic potential (EPSP) depression. The D1 receptor agonist SKF81297 (5 mu M) significantly reduced the amplitude of the first EPSP but not of subsequent responses in EPSP trains, which still displayed significant depression. Dopamine (DA; 10 mu M) effects were similar to those of SKF81297 and were abolished by the D1 antagonist SCH23390 (5 mu M), indicating a D1 receptor-mediated effect. DA did not alter miniature excitatory postsynaptic currents, suggesting that its effects were activity dependent and presynaptic action potential dependent. In contrast to previous findings in pyramidal neurons, in fast-spiking cells, contribution of N-methyl-D-aspartate receptors to EPSPs at subthreshold potentials was not significant and fast-spiking cell depolarization decreased EPSP duration. In addition, DA had no significant effects on temporal summation. The selective decrease in the amplitude of the first EPSP in trains delivered every 10 s suggests that in fast-spiking neurons, DA reduces the amplitude of EPSPs evoked at low frequency but not of EPSPs evoked by repetitive stimulation. DA may therefore improve detection of EPSP bursts above background synaptic activity. EPSP bursts displaying short-term depression may transmit spike-timing-dependent temporal codes contained in presynaptic spike trains. Thus DA neuromodulation may increase the signal-to-noise ratio at fast-spiking cell inputs.