TY - JOUR
T1 - Glutamate and N-methyl-D-aspartate affect release from crayfish axon terminals in a voltage-dependent manner
AU - Parnas, H.
AU - Parnas, I.
AU - Ravin, R.
AU - Yudelevitch, B.
PY - 1994/11/22
Y1 - 1994/11/22
N2 - 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.
AB - 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.
KW - feedback inhibition
KW - presynaptic autoreceptors
KW - quantal release
KW - synaptic modulation
UR - http://www.scopus.com/inward/record.url?scp=0027943622&partnerID=8YFLogxK
U2 - 10.1073/pnas.91.24.11586
DO - 10.1073/pnas.91.24.11586
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C2 - 7972107
AN - SCOPUS:0027943622
SN - 0027-8424
VL - 91
SP - 11586
EP - 11590
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
IS - 24
ER -