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本文引用的文献

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Molecular Dissection of Neuroligin 2 and Slitrk3 Reveals an Essential Framework for GABAergic Synapse Development.神经连接蛋白2和Slitrk3的分子剖析揭示了GABA能突触发育的基本框架。
Neuron. 2017 Nov 15;96(4):808-826.e8. doi: 10.1016/j.neuron.2017.10.003. Epub 2017 Oct 26.
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Afferent specific role of NMDA receptors for the circuit integration of hippocampal neurogliaform cells.NMDA受体在海马神经胶质样细胞回路整合中的传入特异性作用。
Nat Commun. 2017 Jul 28;8(1):152. doi: 10.1038/s41467-017-00218-y.
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Differential role of GABA receptors and neuroligin 2 for perisomatic GABAergic synapse formation in the hippocampus.GABA 受体和神经黏附素 2 对海马体周围 GABA 能突触形成的差异作用。
Brain Struct Funct. 2017 Dec;222(9):4149-4161. doi: 10.1007/s00429-017-1462-7. Epub 2017 Jun 22.
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Genetic inhibition of neurotransmission reveals role of glutamatergic input to dopamine neurons in high-effort behavior.遗传抑制神经递质传递揭示了谷氨酸能输入到多巴胺神经元在高努力行为中的作用。
Mol Psychiatry. 2018 May;23(5):1213-1225. doi: 10.1038/mp.2017.7. Epub 2017 Feb 14.
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Distortion of the normal function of synaptic cell adhesion molecules by genetic variants as a risk for autism spectrum disorders.遗传变异导致突触细胞粘附分子正常功能的畸变,这是自闭症谱系障碍的一个风险因素。
Brain Res Bull. 2017 Mar;129:82-90. doi: 10.1016/j.brainresbull.2016.10.006. Epub 2016 Oct 12.
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Regulation of GABAergic synapse development by postsynaptic membrane proteins.突触后膜蛋白对γ-氨基丁酸能突触发育的调控
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γ-Aminobutyric Acid Type A (GABAA) Receptor Subunits Play a Direct Structural Role in Synaptic Contact Formation via Their N-terminal Extracellular Domains.γ-氨基丁酸A型(GABAA)受体亚基通过其N端胞外结构域在突触接触形成中发挥直接的结构作用。
J Biol Chem. 2016 Jul 1;291(27):13926-13942. doi: 10.1074/jbc.M116.714790. Epub 2016 Apr 20.
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An NMDA Receptor-Dependent Mechanism Underlies Inhibitory Synapse Development.一种依赖NMDA受体的机制是抑制性突触发育的基础。
Cell Rep. 2016 Jan 26;14(3):471-478. doi: 10.1016/j.celrep.2015.12.061. Epub 2016 Jan 7.
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Distinct roles of NMDA receptors at different stages of granule cell development in the adult brain.NMDA受体在成人大脑海马颗粒细胞发育不同阶段的独特作用。
Elife. 2015 Oct 16;4:e07871. doi: 10.7554/eLife.07871.
10
Calsyntenins function as synaptogenic adhesion molecules in concert with neurexins.钙结合蛋白与神经配素协同作用,作为突触生成黏附分子发挥功能。
Cell Rep. 2014 Mar 27;6(6):1096-1109. doi: 10.1016/j.celrep.2014.02.010. Epub 2014 Mar 6.

N-甲基-D-天冬氨酸受体的基因缺失抑制了两种不同类型中枢神经元中的γ-氨基丁酸能突触传递。

Genetic deletion of NMDA receptors suppresses GABAergic synaptic transmission in two distinct types of central neurons.

作者信息

Gu Xinglong, Lu Wei

机构信息

Synapse and Neural Circuit Research Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892, USA.

Synapse and Neural Circuit Research Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892, USA.

出版信息

Neurosci Lett. 2018 Mar 6;668:147-153. doi: 10.1016/j.neulet.2018.01.024. Epub 2018 Feb 3.

DOI:10.1016/j.neulet.2018.01.024
PMID:29355693
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6136253/
Abstract

NMDA-type ionotropic glutamate receptors (NMDARs) play an important role in the regulation of synapse development and function in the brain. Recently we have shown that NMDARs are critical for GABAergic synapse development in developing hippocampal neurons. However, it remains unclear whether NMDARs are important for establishment of GABAergic synaptic transmission in other types of neurons in the brain. Here we report that in both cortical pyramidal neurons and midbrain dopamine neurons in ventral tegmental area (VTA), genetic deletion of the GluN1 subunit, which is required for assembly of functional NMDARs, leads to a strong reduction of GABAergic synaptic transmission. These data demonstrate that NMDARs play an important role in the development of GABAergic synaptic transmission in two types of neurons with distinct developmental origins, and suggest that NMDARs are commonly involved in development of GABAergic synaptic transmission in different types of neurons in the brain.

摘要

N-甲基-D-天冬氨酸(NMDA)型离子otropic谷氨酸受体(NMDARs)在大脑突触发育和功能的调节中起重要作用。最近我们发现,NMDARs对发育中的海马神经元的GABA能突触发育至关重要。然而,NMDARs对大脑中其他类型神经元的GABA能突触传递的建立是否重要仍不清楚。在这里我们报告,在皮层锥体神经元和腹侧被盖区(VTA)的中脑多巴胺神经元中,功能性NMDARs组装所必需的GluN1亚基的基因缺失导致GABA能突触传递的强烈减少。这些数据表明,NMDARs在具有不同发育起源的两种神经元的GABA能突触传递发育中起重要作用,并表明NMDARs通常参与大脑中不同类型神经元的GABA能突触传递发育。