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When are class I metabotropic glutamate receptors necessary for long-term potentiation?I 类代谢型谷氨酸受体在何时对长时程增强是必需的?
J Neurosci. 1998 Aug 15;18(16):6071-80. doi: 10.1523/JNEUROSCI.18-16-06071.1998.
2
(+)-MCPG blocks induction of LTP in CA1 of rat hippocampus via agonist action at an mGluR group II receptor.(+)-α-甲基-4-羧基苯甘氨酸通过作用于代谢型谷氨酸受体II组的激动剂,阻断大鼠海马体CA1区的长时程增强诱导。
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3
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4
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Transient translocation of protein kinase Cgamma in hippocampal long-term potentiation depends on activation of metabotropic glutamate receptors.蛋白激酶Cγ在海马体长期增强中的瞬时易位取决于代谢型谷氨酸受体的激活。
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10
Metabotropic glutamate receptor antagonist, (R,S)-alpha-methyl-4-carboxyphenyglycine, blocks two distinct forms of long-term potentiation in area CA1 of rat hippocampus.代谢型谷氨酸受体拮抗剂(R,S)-α-甲基-4-羧基苯甘氨酸可阻断大鼠海马CA1区两种不同形式的长时程增强。
Neurosci Lett. 1995 Dec 1;201(1):73-6. doi: 10.1016/0304-3940(95)12141-p.

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本文引用的文献

1
A monoclonal antibody shows discrete cellular and subcellular localizations of mGluR1 alpha metabotropic glutamate receptors.一种单克隆抗体显示了代谢型谷氨酸受体mGluR1α在细胞和亚细胞水平的离散定位。
J Chem Neuroanat. 1997 Jul;13(2):77-93. doi: 10.1016/s0891-0618(97)00023-9.
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Potentiation of synaptic transmission in the rat dentate gyrus in vitro by (S)-3,5-dihydroxyphenylglycine ((S)-DHPG).(S)-3,5-二羟基苯甘氨酸((S)-DHPG)对体外培养的大鼠齿状回突触传递的增强作用
Neurosci Lett. 1997 Jun 20;229(1):29-32. doi: 10.1016/s0304-3940(97)00404-7.
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Mice lacking metabotropic glutamate receptor 5 show impaired learning and reduced CA1 long-term potentiation (LTP) but normal CA3 LTP.缺乏代谢型谷氨酸受体5的小鼠表现出学习能力受损以及CA1区长期增强效应(LTP)减弱,但CA3区LTP正常。
J Neurosci. 1997 Jul 1;17(13):5196-205. doi: 10.1523/JNEUROSCI.17-13-05196.1997.
4
Pharmacology and functions of metabotropic glutamate receptors.代谢型谷氨酸受体的药理学与功能
Annu Rev Pharmacol Toxicol. 1997;37:205-37. doi: 10.1146/annurev.pharmtox.37.1.205.
5
Metabotropic glutamate receptor dependent EPSP and EPSP-spike potentiation in area CA1 of the submerged rat hippocampal slice.代谢型谷氨酸受体依赖性兴奋性突触后电位及在浸没的大鼠海马脑片CA1区的兴奋性突触后电位-锋电位增强
J Neurophysiol. 1996 Nov;76(5):3126-35. doi: 10.1152/jn.1996.76.5.3126.
6
Metabotropic glutamate receptor subtype agonists facilitate long-term potentiation within a distinct time window in the dentate gyrus in vivo.代谢型谷氨酸受体亚型激动剂在体内齿状回的特定时间窗内促进长时程增强。
Neuroscience. 1996 Oct;74(3):723-31. doi: 10.1016/0306-4522(96)00162-5.
7
Metabotropic glutamate receptor antagonist, (R,S)-alpha-methyl-4-carboxyphenyglycine, blocks two distinct forms of long-term potentiation in area CA1 of rat hippocampus.代谢型谷氨酸受体拮抗剂(R,S)-α-甲基-4-羧基苯甘氨酸可阻断大鼠海马CA1区两种不同形式的长时程增强。
Neurosci Lett. 1995 Dec 1;201(1):73-6. doi: 10.1016/0304-3940(95)12141-p.
8
Long-term depression in rat visual cortex is associated with a lower rise of postsynaptic calcium than long-term potentiation.大鼠视觉皮层中的长时程抑制与突触后钙的升高幅度低于长时程增强有关。
Neurosci Res. 1996 Feb;24(3):265-74. doi: 10.1016/0168-0102(95)01001-7.
9
Class I metabotropic glutamate receptor agonists do not facilitate the induction of long-term potentiation in the dentate gyrus of the rat in vitro.I 类代谢型谷氨酸受体激动剂不能促进体外培养的大鼠齿状回长时程增强的诱导。
Neurosci Lett. 1995 Dec 29;202(1-2):73-6. doi: 10.1016/0304-3940(95)12202-8.
10
Postsynaptic levels of [Ca2+]i needed to trigger LTD and LTP.触发长时程抑制(LTD)和长时程增强(LTP)所需的突触后钙离子浓度([Ca2+]i)水平。
Neuron. 1996 Mar;16(3):619-29. doi: 10.1016/s0896-6273(00)80081-1.

I 类代谢型谷氨酸受体在何时对长时程增强是必需的?

When are class I metabotropic glutamate receptors necessary for long-term potentiation?

作者信息

Wilsch V W, Behnisch T, Jäger T, Reymann K G, Balschun D

机构信息

Leibniz Institute for Neurobiology, Department of Neurophysiology, D-39008 Magdeburg, Germany.

出版信息

J Neurosci. 1998 Aug 15;18(16):6071-80. doi: 10.1523/JNEUROSCI.18-16-06071.1998.

DOI:10.1523/JNEUROSCI.18-16-06071.1998
PMID:9698302
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6793202/
Abstract

The involvement of metabotropic glutamate receptors (mGluRs) in hippocampal long-term potentiation (LTP) is a matter of controversial debate. Using [Ca2+]i measurements by confocal laser scanning microscopy and field recordings of EPSPs (fEPSPs) in the hippocampal CA1-region, we found that the efficacy of the broad-spectrum mGluR-antagonist (S)-alpha-methyl-4-carboxyphenylglycine (MCPG) and of (S)-4-carboxy-phenylglycine (4-CPG), a selective antagonist at class I mGluRs, in LTP is contingent on the tetanization strength and the resulting [Ca2+]i response. As indicated by experiments in which we blocked voltage-dependent calcium channels (VDCCs) and intracellular Ca2+ stores (ICSs), the functional significance of class I mGluRs in LTP is confined to certain types of potentiation, which are induced by weak tetanization protocols and require the release of Ca2+ from ICSs for induction. During strong tetanic stimulation, this Ca2+ source is functionally bypassed by activating VDCCs.

摘要

代谢型谷氨酸受体(mGluRs)参与海马体长期增强效应(LTP)是一个存在争议的话题。通过共聚焦激光扫描显微镜测量[Ca2+]i以及记录海马体CA1区的兴奋性突触后电位(fEPSPs),我们发现广谱mGluR拮抗剂(S)-α-甲基-4-羧基苯甘氨酸(MCPG)和I类mGluRs的选择性拮抗剂(S)-4-羧基苯甘氨酸(4-CPG)对LTP的作用效果取决于强直刺激强度以及由此产生的[Ca2+]i反应。我们通过阻断电压依赖性钙通道(VDCCs)和细胞内钙库(ICSs)的实验表明,I类mGluRs在LTP中的功能意义仅限于某些类型的增强效应,这些增强效应由弱强直刺激方案诱导,并且诱导过程需要从ICSs中释放Ca2+。在强强直刺激期间,通过激活VDCCs,这种Ca2+来源在功能上被绕过。