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Mechanism of presynaptic inhibition by neuropeptide Y at sympathetic nerve terminals

Nature volume 364, pages 635–639 (1993)Cite this article

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.

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Author notes

  1. David Bleakman

    Present address: Lilly Research centre, Erl Wood Manor, Windlesham, Surrey, GU OPH, UK

  2. William F. Colmers: Department of Pharmacology, University of Alberta, Edmonton, Alberta T6G 2H7, Canada

  3. Richard J. Miller: To whom correspondenc should be addressed.

Authors and Affiliations

  1. Department of Pharmacological and Physiological Sciences, University of Chicago, 947 East 58th Street, Chicago, Illinois, 60637, USA

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

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  1. Peter T. Toth
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Toth, P., Bindokas, V., Bleakman, D. et al. Mechanism of presynaptic inhibition by neuropeptide Y at sympathetic nerve terminals. Nature 364, 635–639 (1993). https://doi.org/10.1038/364635a0

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