Mechanism of presynaptic inhibition by neuropeptide Y at sympathetic nerve terminals

Nature. 1993 Aug 12;364(6438):635-9. doi: 10.1038/364635a0.


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 noradrenaline act as cotransmitters at many sympathetic synapses. Both of these substances produce presynaptic inhibition and can inhibit Ca2+ currents in the soma of sympathetic neurons. 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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Action Potentials / physiology
  • Animals
  • Calcium Channel Blockers / pharmacology
  • Calcium Channels / drug effects
  • Calcium Channels / physiology*
  • Cells, Cultured
  • Ganglia, Sympathetic / cytology
  • Nerve Endings / drug effects
  • Nerve Endings / physiology*
  • Neural Inhibition / physiology*
  • Neuropeptide Y / physiology*
  • Peptides / pharmacology
  • Rats
  • Sympathetic Nervous System / drug effects
  • Sympathetic Nervous System / physiology*
  • Synapses / physiology
  • omega-Conotoxin GVIA


  • Calcium Channel Blockers
  • Calcium Channels
  • Neuropeptide Y
  • Peptides
  • omega-Conotoxin GVIA