1983British Journal of PharmacologyOpen access

In vivo release of [3H]‐purines by quinolinic acid and related compounds

M.N. Perkins, Trevor W. Stone

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Abstract

In vivo release of [3H]-purines from the cortex of anaesthetized rats was measured and the actions of excitatory amino acids and analogues investigated. High KCl, N-methyl-DL-aspartate (NMDLA) and quinolinic acid produced a large increase in basal release of labelled materials. Glutamate, quisqualate and kainate had less effect. The N-methyl-D-aspartic acid (NMDA)-preferring receptor antagonist, 2-amino-7-phosphonohepatanoic acid, significantly reduced the release evoked by NMDLA and quinolinate but not that produced by the other agonists. Kynurenic acid, a compound metabolically related to quinolinic acid, reduced the release due to NMDLA and quinolinate but not glutamate. The results add further support to the suggestion that quinolinic acid acts on the NMDA-preferring receptor.

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In vivo release of [3H]-purines from the cortex of anaesthetized rats was measured and the actions of excitatory amino acids and analogues investigated. High KCl, N-methyl-DL-aspartate (NMDLA) and quinolinic acid produced a large increase in basal release of labelled materials. Glutamate, quisqualate and kainate had less effect. The N-methyl-D-aspartic acid (NMDA)-preferring receptor antagonist, 2-amino-7-phosphonohepatanoic acid, significantly reduced the release evoked by NMDLA and quinolinate but not that produced by the other agonists. Kynurenic acid, a compound metabolically related to quinolinic acid, reduced the release due to NMDLA and quinolinate but not glutamate. The results add further support to the suggestion that quinolinic acid acts on the NMDA-preferring receptor.

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Available abstract

In vivo release of [3H]-purines from the cortex of anaesthetized rats was measured and the actions of excitatory amino acids and analogues investigated. High KCl, N-methyl-DL-aspartate (NMDLA) and quinolinic acid produced a large increase in basal release of labelled materials. Glutamate, quisqualate and kainate had less effect. The N-methyl-D-aspartic acid (NMDA)-preferring receptor antagonist, 2-amino-7-phosphonohepatanoic acid, significantly reduced the release evoked by NMDLA and quinolinate but not that produced by the other agonists. Kynurenic acid, a compound metabolically related to quinolinic acid, reduced the release due to NMDLA and quinolinate but not glutamate. The results add further support to the suggestion that quinolinic acid acts on the NMDA-preferring receptor.

Key concepts: Quinolinic acid, Quinolinate, Kynurenic acid, NMDA receptor, Kainate receptor, Quisqualic acid, Glutamate receptor, Chemistry

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