Agonists that suppress M-current elicit phosphoinositide turnover and Ca2+ transients, but these events do not explain M-current suppression

Paul J. Pfaffinger, Mark D. Leibowitz, Emily M. Subers, Neil M. Nathanson, Wolfhard Almers, Bertil Hille

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Abstract

The hypothesis that acetylcholine, substance P, and LHRH suppress M-current by activating phospholipase C was tested. Each agonist caused turnover of phosphoinositide, as measured by release of inositol phosphates, and a modest transient rise in intracellular free Ca2+ ([Ca2+]i), as determined with fura-2. Active phorhol esters depressed M-current only 50% and did not prevent further suppression by LHRH. M-current, its control by agonists, and its depression by phorbol esters were not affected by adding inositol trisphosphate or Ca2+ buffers with high or low Cal+ to the whole-cell, voltage-clamp pipette. We conclude that phospholipase C activation does occur but does not mediate the suppression of M-current by agonists. Caffeine produced large [Ca2+]i transients and acted as an agonist to suppress M-current.

Original languageEnglish (US)
Pages (from-to)477-484
Number of pages8
JournalNeuron
Volume1
Issue number6
DOIs
StatePublished - Aug 1988

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ASJC Scopus subject areas

  • Neuroscience(all)

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