Glutamate and N-methyl-D-aspartate affect release from crayfish axon terminals in a voltage-dependent manner

H. Parnas*, I. Parnas, R. Ravin, B. Yudelevitch

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

34 Scopus citations

Abstract

In the crayfish neuromuscular junction, the excitatory transmitter is glutamate. The present study shows that at concentrations as low as 5 x 10- 7 M, glutamate affects the depolarization-evoked release of neurotransmitter. Furthermore, the effect of glutamate on release is voltage- dependent and depends on the level of the depolarizing pulse. Nerve terminals were exposed to 5 x 10-7 M tetrodotoxin and then depolarized to different levels by a macropatch electrode. Depending on the amplitude of the depolarizing pulse, glutamate (5 x 10-7 to 1 x 10-5 M) had a dual effect on release. At small depolarizing pulses, glutamate reduced release, whereas at large depolarizing pulses, it enhanced it. Glutamate at 10-6 M had no significant effect on action-potential-induced release. At 10-4 M glutamate, the action-potential-induced release was always inhibited. N- Methyl-D-aspartate was found to mimic one of the effects of glutamate: N- methyl-D-aspartate (10-7 to 10-5 M) reduced release at small depolarizing pulses but had no effect with larger depolarizations. 2-Amino-5- phosphonovaleric acid blocked the effect of N-methyl-D-aspartate.

Original languageEnglish
Pages (from-to)11586-11590
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume91
Issue number24
DOIs
StatePublished - 22 Nov 1994

Keywords

  • feedback inhibition
  • presynaptic autoreceptors
  • quantal release
  • synaptic modulation

Fingerprint

Dive into the research topics of 'Glutamate and N-methyl-D-aspartate affect release from crayfish axon terminals in a voltage-dependent manner'. Together they form a unique fingerprint.

Cite this