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1S,3S-氨基环丙烷羧酸对高频刺激诱导的齿状回长时程增强的阻断作用:进一步证明长时程增强不能作为学习模型的证据

Block of HFS-induced LTP in the dentate gyrus by 1S,3S-ACPD: further evidence against LTP as a model for learning.

作者信息

Hölscher C, Anwyl R, Rowan M

机构信息

Department of Pharmacology, Trinity College, Dublin, Republic of Ireland.

出版信息

Neuroreport. 1997 Jan 20;8(2):451-4. doi: 10.1097/00001756-199701200-00015.

DOI:10.1097/00001756-199701200-00015
PMID:9080427
Abstract

We have previously shown that block of high-frequency stimulation (HFS) induced long-term potentiation (LTP) of synaptic transmission in area CA1 by (1S,3S)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3S-ACPD; 5 microliters of a 20 mM solution), an agonist at group II metabotropic glutamate receptors, did not prevent animals from learning a spatial task. Here we show that the same dose of 1S,3S-ACPD also blocked the induction of HFS-induced LTP of the slope of the excitatory postsynaptic potential and of the amplitude of the population spike in the dentate gyrus. We conclude that HFS-induced LTP in the dentate gyrus is not a good model for memory formation.

摘要

我们之前已经表明,通过II组代谢型谷氨酸受体激动剂(1S,3S)-1-氨基环戊烷-1,3-二羧酸(1S,3S-ACPD;5微升20毫摩尔溶液)阻断高频刺激(HFS)诱导的海马CA1区突触传递长时程增强(LTP),并不会妨碍动物学习空间任务。在此我们表明,相同剂量的1S,3S-ACPD也阻断了HFS诱导的齿状回兴奋性突触后电位斜率和群体峰电位幅度的LTP诱导。我们得出结论,HFS诱导的齿状回LTP不是记忆形成的良好模型。

相似文献

1
Block of HFS-induced LTP in the dentate gyrus by 1S,3S-ACPD: further evidence against LTP as a model for learning.1S,3S-氨基环丙烷羧酸对高频刺激诱导的齿状回长时程增强的阻断作用:进一步证明长时程增强不能作为学习模型的证据
Neuroreport. 1997 Jan 20;8(2):451-4. doi: 10.1097/00001756-199701200-00015.
2
HFS-induced long-term potentiation and LFS-induced depotentiation in area CA1 of the hippocampus are not good models for learning.高频刺激诱导的海马体CA1区长期增强效应和低频刺激诱导的去增强效应并非学习的良好模型。
Psychopharmacology (Berl). 1997 Mar;130(2):174-82. doi: 10.1007/s002130050226.
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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.
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Priming of long-term potentiation by prior activation of group I and II metabotropic glutamate receptors in the rat dentate gyrus in vitro.通过体外预先激活大鼠齿状回中的I组和II组代谢型谷氨酸受体引发长时程增强效应。
Brain Res. 1998 Oct 26;809(1):91-6. doi: 10.1016/s0006-8993(98)00897-x.
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Block of theta-burst-induced long-term potentiation by (1S,3S)-1-aminocyclopentane-1,3-dicarboxylic acid: further evidence against long-term potentiation as a model for learning.(1S,3S)-1-氨基环戊烷-1,3-二羧酸对θ波爆发诱导的长时程增强的阻断作用:进一步证明长时程增强并非学习的模型。
Neuroscience. 1997 Nov;81(1):17-22. doi: 10.1016/s0306-4522(97)00183-8.
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Analysis of the interaction between arachidonic acid and metabotropic glutamate receptor activation reveals that phospholipase C acts as a coincidence detector in the expression of long-term potentiation in the rat dentate gyrus.对花生四烯酸与代谢型谷氨酸受体激活之间相互作用的分析表明,磷脂酶C在大鼠齿状回长时程增强的表达中充当一种巧合探测器。
Hippocampus. 1998;8(1):48-56. doi: 10.1002/(SICI)1098-1063(1998)8:1<48::AID-HIPO5>3.0.CO;2-3.
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Activation of metabotropic glutamate receptors induce differential effects on synaptic transmission in the dentate gyrus and CA1 of the hippocampus in the anaesthetized rat.代谢型谷氨酸受体的激活对麻醉大鼠海马齿状回和CA1区的突触传递产生不同影响。
Neuropharmacology. 1996 Mar;35(3):337-46. doi: 10.1016/0028-3908(95)00185-9.
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1S,3R-ACPD dose dependently induces a slow onset potentiation in the dentate gyrus in vivo.
Eur J Pharmacol. 1995 Dec 29;294(2-3):497-503. doi: 10.1016/0014-2999(95)00579-x.
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Activation of group-II metabotropic glutamate receptors blocks induction of long-term potentiation and depotentiation in area CA1 of the rat in vivo.II 型代谢型谷氨酸受体的激活可阻断大鼠体内 CA1 区的长时程增强和长时程抑制的诱导。
Eur J Pharmacol. 1997 Mar 19;322(2-3):155-63. doi: 10.1016/s0014-2999(96)01000-x.
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(+)-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。
J Neurophysiol. 1998 Mar;79(3):1270-6. doi: 10.1152/jn.1998.79.3.1270.

引用本文的文献

1
Stimulation on the positive phase of hippocampal theta rhythm induces long-term potentiation that can Be depotentiated by stimulation on the negative phase in area CA1 in vivo.对海马θ节律正相的刺激可诱导长时程增强,在活体中,CA1区负相的刺激可使其去增强。
J Neurosci. 1997 Aug 15;17(16):6470-7. doi: 10.1523/JNEUROSCI.17-16-06470.1997.