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本文引用的文献

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Front Cell Neurosci. 2024 Jul 24;18:1414955. doi: 10.3389/fncel.2024.1414955. eCollection 2024.
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Cortical parvalbumin neurons are responsible for homeostatic sleep rebound through CaMKII activation.皮质层 parvalbumin 神经元通过 CaMKII 的激活对睡眠内稳态反弹起作用。
Nat Commun. 2024 Jul 18;15(1):6054. doi: 10.1038/s41467-024-50168-5.
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Keeping Your Brain in Balance: Homeostatic Regulation of Network Function.保持大脑平衡:网络功能的稳态调节
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Altered Associations Between Task Performance and Dorsolateral Prefrontal Cortex Activation During Cognitive Control in Schizophrenia.精神分裂症患者认知控制过程中任务表现与背外侧前额叶皮层激活之间的改变关联。
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Mechanisms regulating the properties of inhibition-based gamma oscillations in primate prefrontal and parietal cortices.调节灵长类前额叶和顶叶皮层基于抑制的γ振荡特性的机制。
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CaMKIIα Promoter-Controlled Circuit Manipulations Target Both Pyramidal Cells and Inhibitory Interneurons in Cortical Networks.CaMKIIα 启动子控制的电路操作靶向皮质网络中的锥体神经元和抑制性中间神经元。
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Spike timing-dependent plasticity and memory.时相关突触可塑性与记忆。
Curr Opin Neurobiol. 2023 Jun;80:102707. doi: 10.1016/j.conb.2023.102707. Epub 2023 Mar 14.
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HCN channels at the cell soma ensure the rapid electrical reactivity of fast-spiking interneurons in human neocortex.HCN 通道位于细胞体,确保了人类新皮层中快速放电中间神经元的快速电反应性。
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9
Strength of Excitatory Inputs to Layer 3 Pyramidal Neurons During Synaptic Pruning in the Monkey Prefrontal Cortex: Relevance for the Pathogenesis of Schizophrenia.在猴子前额皮质的突触修剪过程中,第 3 层锥体神经元的兴奋性输入强度:与精神分裂症发病机制的相关性。
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The plasticitome of cortical interneurons.皮质中间神经元的可塑性组。
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对猴子前额叶皮层神经元兴奋性进行基因操作后锥体细胞的突触改变。

Synaptic alterations in pyramidal cells following genetic manipulation of neuronal excitability in monkey prefrontal cortex.

作者信息

Gonzalez-Burgos Guillermo, Miyamae Takeaki, Nishihata Yosuke, Krimer Olga L, Wade Kirsten, Fish Kenneth N, Arion Dominique, Cai Zhao-Lin, Xue Mingshan, Stauffer William R, Lewis David A

机构信息

Department of Psychiatry, University of Pittsburgh, Pittsburgh, Pennsylvania, United States.

Department of Neuroscience, Baylor College of Medicine, Houston, Texas, United States.

出版信息

J Neurophysiol. 2025 Feb 1;133(2):399-413. doi: 10.1152/jn.00326.2024. Epub 2024 Dec 31.

DOI:10.1152/jn.00326.2024
PMID:39740351
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12208097/
Abstract

The primate dorsolateral prefrontal cortex (DLPFC) displays unique in vivo activity patterns, but how in vivo activity regulates DLPFC pyramidal neuron (PN) properties remains unclear. We assessed the effects of in vivo Kir2.1 overexpression, a genetic silencing tool, on synapses in monkey DLPFC PNs. We show for the first time that recombinant ion channel expression successfully modifies the excitability of primate cortex neurons, producing effects on synaptic properties apparently different from those in the rodent cortex.

摘要

灵长类动物的背外侧前额叶皮质(DLPFC)表现出独特的体内活动模式,但体内活动如何调节DLPFC锥体神经元(PN)的特性仍不清楚。我们评估了一种基因沉默工具——体内过表达Kir2.1对猴DLPFC锥体神经元突触的影响。我们首次表明,重组离子通道的表达成功改变了灵长类动物皮质神经元的兴奋性,对突触特性产生的影响明显不同于啮齿动物皮质。