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Inhibition of spontaneous EPSCs and IPSCs by presynaptic GABAB receptors on rat supraoptic magnocellular neurons.大鼠视上核大细胞神经元上突触前GABAB受体对自发性兴奋性突触后电流和抑制性突触后电流的抑制作用。
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GABAB receptor-mediated inhibition of spontaneous inhibitory synaptic currents in rat midbrain culture.GABAB受体介导对大鼠中脑培养物中自发性抑制性突触电流的抑制作用。
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本文引用的文献

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Synaptic interactions between mammalian central neurons in cell culture. II. Quantal Analysis of EPSPs.细胞培养中哺乳动物中枢神经元之间的突触相互作用。II. 兴奋性突触后电位的量子分析。
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A bicuculline-resistant inhibitory post-synaptic potential in rat hippocampal pyramidal cells in vitro.体外培养的大鼠海马锥体细胞中一种对荷包牡丹碱有抗性的抑制性突触后电位
J Physiol. 1984 Mar;348:239-54. doi: 10.1113/jphysiol.1984.sp015107.
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Direct hyperpolarizing action of baclofen on hippocampal pyramidal cells.巴氯芬对海马锥体细胞的直接超极化作用。
Nature. 1984;308(5958):450-2. doi: 10.1038/308450a0.
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gamma-aminobutyric acid B receptors are negatively coupled to adenylate cyclase in brain, and in the cerebellum these receptors may be associated with granule cells.γ-氨基丁酸B受体在脑中与腺苷酸环化酶负偶联,在小脑中这些受体可能与颗粒细胞相关。
Mol Pharmacol. 1984 Jan;25(1):24-8.
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Coexistence of GABAA and GABAB receptors on A delta and C primary afferents.Aδ和C类初级传入纤维上GABAA和GABAB受体的共存。
Br J Pharmacol. 1984 Feb;81(2):327-33. doi: 10.1111/j.1476-5381.1984.tb10082.x.
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Inhibition of GABAB receptor binding by guanyl nucleotides.鸟苷酸对GABAB受体结合的抑制作用。
J Neurochem. 1984 Mar;42(3):652-7. doi: 10.1111/j.1471-4159.1984.tb02732.x.
7
Baclofen selectively inhibits transmission at synapses made by axons of CA3 pyramidal cells in the hippocampal slice.巴氯芬可选择性抑制海马切片中CA3锥体细胞轴突形成的突触处的信号传递。
J Pharmacol Exp Ther. 1982 Nov;223(2):291-7.
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Two types of gamma-aminobutyric acid receptor on embryonic sensory neurones.胚胎感觉神经元上的两种γ-氨基丁酸受体
Br J Pharmacol. 1981 Nov;74(3):579-85. doi: 10.1111/j.1476-5381.1981.tb10467.x.
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Improved patch-clamp techniques for high-resolution current recording from cells and cell-free membrane patches.用于从细胞和无细胞膜片进行高分辨率电流记录的改进膜片钳技术。
Pflugers Arch. 1981 Aug;391(2):85-100. doi: 10.1007/BF00656997.
10
3H-baclofen and 3H-GABA bind to bicuculline-insensitive GABA B sites in rat brain.3H-巴氯芬和3H-γ-氨基丁酸与大鼠脑中对荷包牡丹碱不敏感的γ-氨基丁酸B位点结合。
Nature. 1981 Mar 12;290(5802):149-52. doi: 10.1038/290149a0.

关于巴氯芬对培养的大鼠海马神经元之间抑制性突触的突触前作用。

On the presynaptic action of baclofen at inhibitory synapses between cultured rat hippocampal neurones.

作者信息

Harrison N L

机构信息

Laboratory of Neurophysiology, NINDS, National Institutes of Health, Bethesda, MD 20892.

出版信息

J Physiol. 1990 Mar;422:433-46. doi: 10.1113/jphysiol.1990.sp017993.

DOI:10.1113/jphysiol.1990.sp017993
PMID:2352187
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1190141/
Abstract
  1. (-)Baclofen reduces inhibitory postsynaptic potentials (IPSPs) and the associated synaptic currents (IPSCs) at inhibitory GABAergic synapses between cultured rat hippocampal neurones. The reversal potential for the IPSC is unaltered. 2. The effect of (-)baclofen is concentration dependent; the EC50 for (-)baclofen is approximately 5 microM. 3. Statistical analyses of the amplitude fluctuations of the IPSC in the presence of (-)baclofen suggested a presynaptic location for the depression of synaptic transmission by (-)baclofen. In control experiments, lowering extracellular Ca2+ produced similar effects. (-)Baclofen has no detectable postsynaptic actions in these cultured neurones. 4. Phaclofen (0.2-0.5 mM) increases IPSC amplitude but does not significantly block the depressant effect of (-)baclofen on synaptic transmission. 5. The effect of (-)baclofen is not blocked by pertussis toxin pre-treatment. 6. It is concluded that (-)baclofen acts presynaptically to reduce the release of GABA. The mechanism by which release is reduced may involve a phaclofen-insensitive GABAB receptor.
摘要
  1. (-)巴氯芬可降低培养的大鼠海马神经元之间抑制性γ-氨基丁酸(GABA)能突触处的抑制性突触后电位(IPSPs)及相关的突触电流(IPSCs)。IPSC的反转电位未改变。2. (-)巴氯芬的作用呈浓度依赖性;(-)巴氯芬的半数有效浓度(EC50)约为5微摩尔。3. 对存在(-)巴氯芬时IPSC幅度波动的统计分析表明,(-)巴氯芬对突触传递的抑制作用位于突触前。在对照实验中,降低细胞外钙离子浓度产生了类似的效果。在这些培养的神经元中,(-)巴氯芬没有可检测到的突触后作用。4. 苯氯芬(0.2 - 0.5毫摩尔)可增加IPSC幅度,但不能显著阻断(-)巴氯芬对突触传递的抑制作用。5. (-)巴氯芬的作用不会被百日咳毒素预处理所阻断。6. 得出的结论是,(-)巴氯芬通过作用于突触前以减少GABA的释放。释放减少的机制可能涉及一种对苯氯芬不敏感的GABAB受体。