Role of calcium-activated potassium channels in transmitter release at the squid giant synapse.

Published

Journal Article

1. Several compounds known to block Ca2+-activated K+ channels were microinjected into squid 'giant' presynaptic terminals to test the hypothesis that these channels mediate Ca2+-dependent neurotransmitter release. 2. Injection of tetrapentylammonium, nonyl-triethylammonium and decamethonium all reversibly blocked transmission evoked by presynaptic action potentials. 3. All three of these compounds blocked presynaptic Ca2+ channels. The actions of tetrapentylammonium on presynaptic Ca2+ influx were examined in detail and found to be quantitatively sufficient to account for the ability of this compound to inhibit transmitter release. 4. Injection of Ba2+, another agent known to block Ca2+-activated K+ channels, also reversibly blocked evoked transmitter release. Ba2+ simultaneously enhanced basal (asynchronous) transmitter release and thus may be decreasing evoked release by depleting transmitter quanta available for release. 5. None of these results provide any support for the hypothesis that Ca2+-activated K+ channels mediate Ca2+-dependent release of transmitter at the squid synapse. However, our results have identified a new class of compounds that block Ca2+ channels from their cytoplasmic surface.

Full Text

Cited Authors

  • Augustine, GJ; Charlton, MP; Horn, R

Published Date

  • April 1, 1988

Published In

Volume / Issue

  • 398 /

Start / End Page

  • 149 - 164

PubMed ID

  • 2455797

Pubmed Central ID

  • 2455797

Electronic International Standard Serial Number (EISSN)

  • 1469-7793

International Standard Serial Number (ISSN)

  • 0022-3751

Digital Object Identifier (DOI)

  • 10.1113/jphysiol.1988.sp017035

Language

  • eng