Inactivation kinetics of voltage-gated calcium channels in glutamatergic neurons are influenced by SNAP-25

Steven B. Condliffe, Michela Matteoli

Research output: Contribution to journalArticlepeer-review


SNAP-25 forms part of the SNARE core complex that mediates membrane fusion. Biochemical and electrophysiological evidence supports an accessory role for SNAP-25 in interacting with voltage-gated calcium channels (VGCCs) to modulate channel activity. We recently reported that endogenous SNAP-25 negatively regulates VGCC activity in glutamatergic neurons from rat hippocampal cultures by shifting the voltage-dependence of inactivation of the predominant P/Q-type channel current in these cells. In the present study, we extend these findings by investigating the effect that manipulating endogenous SNAP-25 expression has on the inactivation kinetics of VGCC current in both glutamatergic and GABAergic cells recorded from 9-13 DIV cultures. Silencing SNAP-25 in glutamatergic neurons significantly slowed the inactivation rate of P/Q-type VGCC current whereas alterations in SNAP-25 expression did not alter inactivation rates in GABAergic neurons. These results indicate that endogenous SNAP-25 plays an important role in P/Q-type channel regulation in glutamatergic neurons.

Original languageEnglish
Issue number4
Publication statusPublished - Jul 2011


  • GABAergic
  • Glutamatergic
  • Hippocampal neurons
  • Inactivation
  • Kinetics
  • SNAP-25
  • Voltage-gated calcium channels

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry


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