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Glutamate Depresses Release by Activating Non‐conventional Glutamate Receptors at Crayfish Nerve Terminals
Author(s) -
Parnas I.,
Dudel J.,
Parnas H.,
Ravin R.
Publication year - 1996
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1996.tb01172.x
Subject(s) - crayfish , glutamate receptor , receptor , neuroscience , chemistry , metabotropic glutamate receptor , nmda receptor , biophysics , biology , biochemistry , ecology
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, Ca 2+ 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 Ca 2+ . 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.