Mechanism of presynaptic inhibition by neuropeptide Y at sympathetic nerve terminals

Peter T. Toth, Vytautas P. Bindokas, David Bleakman, William F. Colmers, Richard J. Miller*

*Corresponding author for this work

Research output: Contribution to journalArticle

129 Scopus citations

Abstract

CALCIUM influx through voltage-sensitive Ca2+ channels is the normal physiological stimulus for the activity-dependent release of neurotransmitters at synaptic contacts. It has been postulated that presynaptic inhibition of transmitter release is due to a reduction in Ca2+ influx at the nerve terminal, which could result from the direct inhibition of Ca2+ channels. Neuropeptide Y and noradren-aline act as cotransmitters at many sympathetic synapses. Both of these substances produce presynaptic inhibition and can inhibit Ca2+ currents in the soma of sympathetic neurons1-5. Here we provide direct evidence that presynaptic inhibition produced by neuropeptide Y at sympathetic nerve terminals is associated with a reduction in Ca2+ influx and that this is due to the selective inhibition of neuronal N-type Ca2+ channels.

Original languageEnglish (US)
Pages (from-to)635-639
Number of pages5
JournalNature
Volume364
Issue number6438
DOIs
StatePublished - Jan 1 1993

ASJC Scopus subject areas

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