Abstract
The major excitatory amino acids, glutamate (Glu) and aspartate (Asp), are thought to act at three receptor subtypes1 in the mammalian central nervous system (CNS). These are termed quisqualate (QA), N-methyl-D-aspartate (NMDA) and kainate (KA) receptors according to the specific agonist properties of these compounds revealed by electrophysiological studies1,2. Although Glu has been shown to stimulate cyclic GMP formation in brain slices3, direct regulation of second messenger systems (cyclic AMP, Ca2+ or inositol phosphates) subsequent to activation of excitatory amino-acid receptors, has not been extensively studied. Here we demonstrate that in striatal neurones, excitatory amino acids, but not inhibitory or non-neuroactive amino acids, induce a three- to fourfold increase in inositol mono-, di- and triphosphate (IP1, IP2, IP3) formation with the relative potency QA > Glu > NMDA, KA. The Glu-evoked formation of inositol phosphates appears to result principally from actions at QA as well as NMDA receptors on striatal neurones. Our results suggest that excitatory amino acids stimulate inositol phosphate formation directly, rather than indirectly by the evoked release and subsequent actions of adenosine4 or acetylcholine5.
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Sladeczek, F., Pin, JP., Récasens, M. et al. Glutamate stimulates inositol phosphate formation in striatal neurones. Nature 317, 717–719 (1985). https://doi.org/10.1038/317717a0
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DOI: https://doi.org/10.1038/317717a0
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