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本文引用的文献

1
GABAB receptor modulation of voltage-sensitive calcium channels in spines and dendrites.GABAB 受体对脊柱和树突中电压敏感性钙通道的调制。
J Neurosci. 2011 Mar 16;31(11):4221-32. doi: 10.1523/JNEUROSCI.4561-10.2011.
2
M1 muscarinic receptors boost synaptic potentials and calcium influx in dendritic spines by inhibiting postsynaptic SK channels.M1 毒蕈碱型乙酰胆碱受体通过抑制突触后 SK 通道来增强树突棘中的突触电位和钙离子内流。
Neuron. 2010 Dec 9;68(5):936-47. doi: 10.1016/j.neuron.2010.09.004.
3
Basal GABA regulates GABA(B)R conformation and release probability at single hippocampal synapses.基底 GABA 调节单个海马突触处 GABA(B)R 构象和释放概率。
Neuron. 2010 Jul 29;67(2):253-67. doi: 10.1016/j.neuron.2010.06.022.
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Competitive regulation of synaptic Ca2+ influx by D2 dopamine and A2A adenosine receptors.D2 多巴胺和 A2A 腺苷受体对突触 Ca2+内流的竞争性调节。
Nat Neurosci. 2010 Aug;13(8):958-66. doi: 10.1038/nn.2592. Epub 2010 Jul 4.
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GABAB receptor constituents revealed by tandem affinity purification from transgenic mice.应用从转基因小鼠中进行的串联亲和纯化来揭示 GABAB 受体成分。
J Biol Chem. 2010 Jul 2;285(27):20625-33. doi: 10.1074/jbc.M109.049700. Epub 2010 Apr 20.
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Native GABA(B) receptors are heteromultimers with a family of auxiliary subunits.天然 GABA(B) 受体是具有一系列辅助亚基的异聚体。
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7
GABAB receptors modulate NMDA receptor calcium signals in dendritic spines.GABAB 受体调节树突棘中 NMDA 受体的钙信号。
Neuron. 2010 Apr 15;66(1):101-13. doi: 10.1016/j.neuron.2010.03.012.
8
The Sushi domains of GABAB receptors function as axonal targeting signals.GABAB 受体的寿司结构域发挥着轴突靶向信号的功能。
J Neurosci. 2010 Jan 27;30(4):1385-94. doi: 10.1523/JNEUROSCI.3172-09.2010.
9
Regulation of cortical microcircuits by unitary GABA-mediated volume transmission.单一GABA介导的容积传递对皮质微回路的调节
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10
Cholinergic modulation of multivesicular release regulates striatal synaptic potency and integration.多泡释放的胆碱能调节可调控纹状体突触效能和整合。
Nat Neurosci. 2009 Sep;12(9):1121-8. doi: 10.1038/nn.2368. Epub 2009 Aug 9.

GABAB 受体对突触功能的调制。

GABAB receptor modulation of synaptic function.

机构信息

Center for Neural Science, New York University, 4 Washington Place, New York, NY 10003, United States.

出版信息

Curr Opin Neurobiol. 2011 Apr;21(2):339-44. doi: 10.1016/j.conb.2011.02.004. Epub 2011 Mar 2.

DOI:10.1016/j.conb.2011.02.004
PMID:21376567
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3092847/
Abstract

Neuromodulators have complex effects on both the presynaptic release and postsynaptic detection of neurotransmitters. Here we describe recent advances in our understanding of synaptic modulation by metabotropic GABAB receptors. By inhibiting multivesicular release from the presynaptic terminal, these receptors decrease the synaptic glutamate signal. GABAB receptors also inhibit the Ca2+ permeability of NMDA receptors to decrease Ca2+ signals in postsynaptic spines. These new findings highlight the importance of GABAB receptors in regulating many aspects of synaptic transmission. They also point to novel questions about the spatiotemporal dynamics and sources of synaptic modulation in the brain.

摘要

神经调质对神经递质的突触前释放和突触后检测都有复杂的影响。在这里,我们描述了我们对代谢型 GABAB 受体调节突触的理解的最新进展。这些受体通过抑制从突触前末梢的多泡释放,减少突触谷氨酸信号。GABAB 受体还抑制 NMDA 受体的 Ca2+通透性,从而减少突触后棘突中的 Ca2+信号。这些新发现强调了 GABAB 受体在调节突触传递的许多方面的重要性。它们还提出了关于大脑中突触调制的时空动态和来源的新问题。