Effects of 17β-estradiol on chemically induced long-term depression

被引：19

作者：

Shiroma, S ^{[1
]}

Yamaguchi, T ^{[1
]}

Kometani, K ^{[1
]}

机构：

[1] Kyushu Inst Technol, Fac Comp Sci & Syst Engn, Iizuka, Fukuoka 8208502, Japan

来源：

NEUROPHARMACOLOGY | 2005年 / 49卷 / 01期

关键词：

synaptic plasticity; long-term depression (LTD); hippocampus; estradiol; (R,S)-3,5-dihydroxyphenylglycine (DHPG); N-methyl-D-aspartate (NMDA);

D O I：

10.1016/j.neuropharm.2005.02.002

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

In this study, we have investigated the effects of 17 beta-estradiol (E2) on chemically induced long-term depression (LTD). LTD was induced by a brief application of N-methyl-D-aspartate (NMDA) or (R,S)-3,5-dihydroxyphenylglycine (DHPG), a group I metabotropic glutamate receptor agonist. Bath application of E2 alone potentiated population excitatory postsynaptic potentials. This potentiation was readily reversed by washing with control saline. The effect of E2 on NMDA-induced LTD was a conversion of LTD to long-term potentiation (LTP). An application of NMDA in the presence of E2 induced LTP. The induction of LTP was inhibited by an inhibitor of calcium/calmodulin dependent protein kinase (CaMKII). The results suggest that E2 potentiates NMDA receptor function and induces an increase in postsynaptic Ca2+ concentration. An increase in postsynaptic Ca2+ concentration activates CaMKII, leading to LTP. In contrast to NMDA-induced LTD, an application of DHPG in the presence of E2 induced significantly larger LTD. The results suggest that E2 potentiates an as yet unidentified process(es) in inducing LTD by an application of DHPG. The effects of E2 both on NMDA-induced and DHPG-induced LTD were suppressed by an estrogen receptor antagonist. (c) 2005 Elsevier Ltd. All rights reserved.

引用

页码：97 / 102

页数：6

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