Carbachol can potentiate N-methyl-d-aspartate responses in the rat hippocampus by a staurosporine and thapsigargin-insensitive mechanism

Jenni Harvey (Lead / Corresponding author), Richard Balasubramaniam, Graham L. Collingridge

    Research output: Contribution to journalArticlepeer-review

    38 Citations (Scopus)

    Abstract

    Experiments were performed to investigate the mechanism underlying the potentiation of N-methyl-d-aspartate (NMDA) responses by carbachol (CCh) in the CA1 region of rat hippocampal slices. CCh (300 nM) potentiated responses to NMDA, but not to α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), in a readily reversible manner. Potentiation occurred in slices treated with 200 nM tetrodotoxin and perfused with Mg2+-free medium. It also occurred in slices treated with either staurosporine (1 μM), which is a potent inhibitor of a variety of protein kinases including protein kinase C (PKC), or thapsigargin (10 μM), which depletes intracellular Ca2+ stores by preventing their refilling. However, CCh-induced potentiation was abolished in slices perfused with Ca2+-free medium. These data suggest that low concentrations of CCh can acutely potentiate NMDA responses in the hippocampus by a Ca2+-sensitive process that is probably independent of both the activation of PKC and the release of Ca2+ from intracellular stores. This mechanism is similar to that underlying the potentiation of NMDA responses by the metabotropic glutamate receptor (mGluR) agonist. aminocyclopentane-1S,3R-dicarboxylic acid (1S,3R-ACPD).

    Original languageEnglish
    Pages (from-to)165-168
    Number of pages4
    JournalNeuroscience Letters
    Volume162
    Issue number1-2
    DOIs
    Publication statusPublished - 12 Nov 1993

    Keywords

    • Ca
    • Ca pool
    • Carbachol
    • Hippocampus
    • Long-term potentiation
    • NMDA receptor
    • Protein kinase

    ASJC Scopus subject areas

    • General Neuroscience

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