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首页> 外文期刊>European Journal of Pharmacology: An International Journal >Arachidonic acid metabolites and the synaptic potentiation evoked by activation of metabotropic glutamate receptors.
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Arachidonic acid metabolites and the synaptic potentiation evoked by activation of metabotropic glutamate receptors.

机译:花生四烯酸代谢产物和代谢型谷氨酸受体的激活引起的突触增强。

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摘要

We have previously shown that coapplication of arachidonic acid (10 microM) and (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD, 50 microM) evokes an enhancement of synaptic transmission in the CA1 region of the rat hippocampal slice. Here we have investigated whether the metabolites of arachidonic acid are implicated in this potentiation. Inclusion of the cyclo-oxygenase inhibitor indomethacin (10 microM) did not block the potentiation induced by coapplication of arachidonic acid and ACPD. However, the presence of either the cyclo-, lipo- and epoxygenase inhibitor 5,8,11,14-eicosatetraynoic acid (ETYA, 20 microM), or the lipoxygenase inhibitor nordihydroguaiaretic acid (10 microM), prevented the long-lasting enhancement. The results suggest that the lipoxygenase and epoxygenase metabolites of arachidonic acid may be involved in the induction of this form of synaptic potentiation.
机译:先前我们已经表明,花生四烯酸(10 microM)和(1S,3R)-1-氨基环戊烷-1,3-二羧酸(ACPD,50 microM)的共同应用引起大鼠海马CA1区突触传递的增强片。在这里,我们研究了花生四烯酸的代谢产物是否与这种增强作用有关。加入环加氧酶抑制剂吲哚美辛(10 microM)不会阻止花生四烯酸和ACPD共同应用诱导的增强作用。但是,无论是环,脂和环氧合酶抑制剂5,8,11,14-二十碳四丁酸(ETYA,20 microM)还是脂氧合酶抑制剂nordihydroguaiaretic酸(10 microM)的存在,都不能持久地增强这种作用。结果表明花生四烯酸的脂氧合酶和环氧合酶代谢产物可能参与这种形式的突触增强。

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