Control of presynaptic function by a persistent Na(+) current

Neuron. 2008 Dec 26;60(6):975-9. doi: 10.1016/j.neuron.2008.10.052.


Little is known about ion channels that regulate the graded, subthreshold properties of nerve terminals. Using the calyx of Held, we demonstrate here a large presynaptic persistent Na(+) current with unusually hyperpolarized activation voltage. This feature allowed the current to determine both the resting potential and resting conductance of the nerve terminal. Calyces express presynaptic glycine receptors whose activation depolarizes the synapse. We found that activation of the persistent Na(+) current was an essential component in the response to glycine. This Na(+) current originated at or very close to the terminal and was sustained even after trains of large spike-like depolarizations. Because Na(+) channels also underlie the presynaptic action potential, we conclude that their action both triggers and modulates exocytosis through control of presynaptic membrane voltage.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Animals, Newborn
  • Brain Stem / cytology
  • Electric Stimulation
  • Glycine / pharmacology
  • In Vitro Techniques
  • Ion Channel Gating / drug effects
  • Membrane Potentials / drug effects
  • Membrane Potentials / physiology
  • Neurons / cytology
  • Neurons / drug effects
  • Neurons / physiology*
  • Patch-Clamp Techniques
  • Presynaptic Terminals / drug effects
  • Presynaptic Terminals / physiology*
  • Rats
  • Rats, Wistar
  • Sodium Channel Blockers / pharmacology
  • Sodium Channels / physiology*
  • Tetrodotoxin / pharmacology


  • Sodium Channel Blockers
  • Sodium Channels
  • Tetrodotoxin
  • Glycine