The mechanism of block of glutamate synapses by dipicolinic acid

Daisuke Yamamoto, Takenori Miyamoto, Masatsugu Oda, Toako Usui, Jun‐Ichi ‐I Fukami

    Research output: Contribution to journalArticle

    Abstract

    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.

    Original languageEnglish
    Pages (from-to)1-6
    Number of pages6
    JournalArchives of Insect Biochemistry and Physiology
    Volume2
    Issue number1
    DOIs
    Publication statusPublished - 1985

    Keywords

    • Tenebrio molitor
    • dipicolinic acid
    • glutamate synapse
    • neuromuscular junction
    • transmitter release

    ASJC Scopus subject areas

    • Physiology
    • Biochemistry
    • Insect Science

    Fingerprint Dive into the research topics of 'The mechanism of block of glutamate synapses by dipicolinic acid'. Together they form a unique fingerprint.

  • Cite this