Presynaptic group I and II metabotropic glutamate receptors oppositely modulate striatal acetylcholine release

This is the authors' abstract. We don't add key points for this paper.

The effect of metabotropic glutamate receptor agonists and antagonists on KCl (20 mm)-induced endogenous acetylcholine release from rat striatal synaptosomes was investigated. The group I agonist (S)-3,5-dihydroxyphenylglycine (DHPG), 1-1000 nm, potentiated in a concentration-dependent way the KCl-induced acetylcholine release, reaching maximal efficacy at 100 nm (+93 +/- 14%). The effect of DHPG (10 nm) was counteracted by coapplication of (7-hydroximino)cyclopropan-b-chromen-1a-carboxylate (CPCCOEt), 10 microm, a metabotropic glutamate receptor type one selective antagonist, and 2-methyl-6-(phenylethynyl)pyridine (MPEP), 10 microm, a metabotropic glutamate receptor type five selective antagonist, but not by application of either antagonist alone. The group II agonist (2S, 1'R, 2'R, 3'R)-2-(2,3-dicarboxycyclopropyl)glycine (DCG-IV), 1-1000 nm, inhibited in a concentration-dependent way the KCl-induced acetylcholine release displaying maximal efficacy at 300 nm (-32 +/- 2%). The effect of DCG-IV 300 nm was counteracted by the group II selective antagonist (2S)-alpha-ethylglutamic acid (EGLU), 300 microm. The group III agonist L-amino-4-phosphonobutyric acid (L-AP4) failed to alter the KCl-induced acetycholine release up to 300 microm. We conclude that metabotropic glutamate receptors belonging to group I and II are located on the axon terminals of striatal cholinergic interneurons, their activation resulting in facilitation and inhibition, respectively, of acetylcholine release.