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The mechanism of block of glutamate synapses by dipicolinic acid
Author(s) -
Yamamoto Daisuke,
Miyamoto Takenori,
Oda Masatsugu,
Usui Toako,
Fukami JunIchi
Publication year - 1985
Publication title -
archives of insect biochemistry and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.576
H-Index - 66
eISSN - 1520-6327
pISSN - 0739-4462
DOI - 10.1002/arch.940020102
Subject(s) - dipicolinic acid , excitatory postsynaptic potential , biophysics , biology , depolarization , glutamate receptor , biochemistry , neurotransmission , postsynaptic potential , hexamethonium , inhibitory postsynaptic potential , stimulation , neuroscience , botany , receptor , spore
The effect of dipicolinic acid (2,6‐pyridine dicarboxylic acid) on the mealworm neuromuscular junction was studied using conventional microelectrode recording techniques. Dipicolinic acid (10 −5 ‐10 −3 M) added to the bathing solution reversibly blocked neuromuscular transmission. The depolarization in response to iontophoretically applied L‐glutamate (glutamate potential) was not affected by dipicolinic acid even when the neurally evoked excitatory postsynaptic potential (EPSP) was totally abolished. Focal extracellular recordings from single synaptic sites revealed that in the presence of 1 x 10 −4 M dipicolinic acid the presynaptic spike was unchanged, but the quantal content for evoked transmitter release was reduced. The calcium‐dependent action potential elicited by direct stimulation of the muscle fiber was not impaired by dipicolinic acid. These results suggest that dipicolinic acid interferes with the transmitter‐releasing mechanism from the presynaptic terminal.