Glutamate Depresses Release by Activating Non‐conventional Glutamate Receptors at Crayfish Nerve Terminals

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Abstract
The present study shows that release of glutamate from crayfish nerve terminals is inhibited at low depolarizing current pulses by glutamate, N-methyl-D-aspartate (NMDA) and quisqualate. These agonists elicit inhibitory effects at concentrations as low as 10-8 M (quisqualate) and 10-7 M (glutamate and NMDA). The NMDA-mediated inhibition is blocked by (±)-2-amino-5-phosphonovaleric acid (APV). The quisqualate-mediated inhibition is blocked by 6-cyano-7-nitroquinoxaline-2, 3-dione (CNQX). Both CNQX and APV are needed to block glutamate-mediated inhibition. The inhibition of release is not accompanied by a detectable change in presynaptic membrane conductance at the secondary branch. Using fura-2, Ca2+ accumulation during repetitive stimulation (100 Hz) was monitored in single release boutons. Inhibition of release, elicited by 10-4 M glutamate, was not associated with a reduction in the accumulation of Ca2+. We show that the glutamate released from a single or a few release boutons during normal activity acts similarly to glutamate added externally, i.e. it inhibits its own release.