Metabotropic glutamate autoreceptors on nerve terminals of crayfish muscle depress or facilitate release.

In lobster and crayfish neuromuscular junctions superfusion of the excitatory transmitter L-glutamate (L-Glu) has been shown to depress release from motor axon terminals. In crayfish the effect depended on the level of depolarization of the terminal, Glu facilitating release when large depolarizing stimuli were applied. The presynaptic inhibition by Glu could be blocked only with a combination of blockers of Glu channels of the AMPA and N-methyl-D-aspartate (NMDA) types. We report that the effects of Glu can be mimicked by superfusion of (1S,3R)-1-aminocyclo-pentane-1.3-dicarboxylic acid (t-ACPD), an agonist of vertebrate metabotropic Glu-receptors. However, in the recent run of experiments the majority of terminals reacted with facilitation of release on superfusion by Glu or t-ACPD, even when the depolarizing stimuli to the terminal or the control rate of release were low. Average facilitation by 5 microM Glu was by a factor of 4.5. Facilitory responses were not blocked by the combination of APV and CNQX, and thus two types of metabotropic receptors seem to be present, their proportion varying for unknown reasons.