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Evidence for involvement of the cGMP-protein kinase G signaling system in the induction of long-term depression, but not long-term potentiation, in the dentate gyrus in vitro.体外实验中，环磷酸鸟苷-蛋白激酶G信号系统参与齿状回长时程抑制而非长时程增强诱导的证据。
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2
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A Role for Nitric Oxide in Long-term Potentiation.一氧化氮在长时程增强中的作用。
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Nitric-oxide-guanylyl-cyclase-dependent and -independent components of multiple forms of long-term synaptic depression.多种形式的长时程突触抑制中一氧化氮-鸟苷酸环化酶依赖性和非依赖性成分
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Evidence for involvement of the neuronal isoform of nitric oxide synthase during induction of long-term potentiation and long-term depression in the rat dentate gyrus in vitro.体外培养的大鼠齿状回中，一氧化氮合酶神经元亚型在长时程增强和长时程抑制诱导过程中发挥作用的证据。
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mGluR II agonist inhibition of LTP induction, and mGluR II antagonist inhibition of LTD induction, in the dentate gyrus in vitro.体外实验中，代谢型谷氨酸受体II激动剂对齿状回中长时程增强诱导的抑制作用，以及代谢型谷氨酸受体II拮抗剂对长时程抑制诱导的抑制作用。
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Induction of LTD in the dentate gyrus in vitro is NMDA receptor independent, but dependent on Ca2+ influx via low-voltage-activated Ca2+ channels and release of Ca2+ from intracellular stores.体外诱导齿状回中的长时程抑制不依赖NMDA受体，但依赖通过低电压激活的Ca2+通道的Ca2+内流以及细胞内钙库的Ca2+释放。
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Nitric oxide facilitates long-term potentiation, but not long-term depression.一氧化氮促进长时程增强，但不促进长时程抑制。
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Nitric oxide acts directly in the presynaptic neuron to produce long-term potentiation in cultured hippocampal neurons.一氧化氮直接作用于突触前神经元，在培养的海马神经元中产生长时程增强效应。
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体外实验中，环磷酸鸟苷-蛋白激酶G信号系统参与齿状回长时程抑制而非长时程增强诱导的证据。

Evidence for involvement of the cGMP-protein kinase G signaling system in the induction of long-term depression, but not long-term potentiation, in the dentate gyrus in vitro.

作者信息

Wu J, Wang Y, Rowan M J, Anwyl R

机构信息

Department of Physiology, Trinity College, Dublin 2, Ireland.

出版信息

J Neurosci. 1998 May 15;18(10):3589-96. doi: 10.1523/JNEUROSCI.18-10-03589.1998.

DOI:10.1523/JNEUROSCI.18-10-03589.1998
PMID:9570790
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6793137/
Abstract

The involvement of the cGMP-protein kinase G (PKG) signaling pathway in the induction of long-term depression (LTD) and long-term potentiation (LTP) was investigated in the medial perforant path of the dentate gyrus in vitro. Low-frequency stimulation (LFS)-induced LTD of field EPSPs was inhibited by bath perfusion of the selective soluble guanylyl cyclase inhibitor 1H-[1,2,4] oxadiazolo[4,3, -a]quinoxalin-1-one (ODQ). LFS-induced LTD of EPSPs and whole-cell patch-clamped EPSCs was also blocked by bath perfusion and postsynaptic intracellular injection, respectively, of the selective PKG inhibitor KT5823. Elevation of intracellular cGMP by perfusion of the cGMP phosphodiesterase inhibitor zaprinast resulted in induction of LTD of field EPSPs and EPSCs. Occlusion experiments showed mutual inhibition between LFS-induced LTD and zaprinast-induced LTD. The zaprinast-induced LTD of field EPSPs was inhibited by perfusion of ODQ and KT5823. In addition, zaprinast-induced LTD of EPSCs was inhibited by postsynaptic application of KT5823. Glutamate receptor stimulation, especially that of metabotropic glutamate receptors (mGluRs), was required for zaprinast-induced LTD, because cessation of test stimulation or perfusion with the mGluR antagonist (+)-alpha-methyl-4-carboxyphenylglycine (MCPG) inhibited zaprinast-induced LTD. No inhibitory effect of ODQ or KT5823 on the induction of LTP of EPSPs or EPSCs was found. These data indicate that the cGMP-guanyly cyclase-PKG signaling pathway in the dentate gyrus is essential for induction of LTD, although not of LTP, in the dentate gyrus.

摘要

在体外研究了环磷酸鸟苷-蛋白激酶G（PKG）信号通路在齿状回内侧穿通通路中长时程抑制（LTD）和长时程增强（LTP）诱导过程中的作用。选择性可溶性鸟苷酸环化酶抑制剂1H-[1,2,4]恶二唑并[4,3,-a]喹喔啉-1-酮（ODQ）的浴灌流抑制了低频刺激（LFS）诱导的场兴奋性突触后电位（fEPSP）的LTD。选择性PKG抑制剂KT5823的浴灌流和突触后细胞内注射分别阻断了LFS诱导的兴奋性突触后电位（EPSP）和全细胞膜片钳记录的兴奋性突触后电流（EPSC）的LTD。环磷酸鸟苷磷酸二酯酶抑制剂扎普司特的灌流使细胞内环磷酸鸟苷升高，导致场EPSP和EPSC的LTD诱导。阻断实验表明LFS诱导的LTD和扎普司特诱导的LTD之间存在相互抑制。ODQ和KT5823的灌流抑制了扎普司特诱导的场EPSP的LTD。此外，突触后应用KT5823抑制了扎普司特诱导的EPSC的LTD。扎普司特诱导的LTD需要谷氨酸受体刺激，尤其是代谢型谷氨酸受体（mGluR）的刺激，因为测试刺激的停止或代谢型谷氨酸受体拮抗剂（+）-α-甲基-4-羧基苯甘氨酸（MCPG）的灌流抑制了扎普司特诱导的LTD。未发现ODQ或KT5823对EPSP或EPSC的LTP诱导有抑制作用。这些数据表明，齿状回中的环磷酸鸟苷-鸟苷酸环化酶-PKG信号通路对于齿状回中LTD的诱导至关重要，尽管对LTP的诱导并非如此。