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Arachidonic acid metabolites and the synaptic potentiation evoked by activation of metabotropic glutamate receptors.

作者信息

Collins D R, Davies S N

机构信息

Department of Biomedical Sciences, Institute of Medical Sciences, University of Aberdeen, Foresterhill, UK.

出版信息

Eur J Pharmacol. 1998 Jan 26;342(2-3):213-6. doi: 10.1016/s0014-2999(97)01590-2.

Abstract

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.

摘要

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