A cell model study of calcium influx mechanism regulated by calcium-dependent potassium channels in Purkinje cell dendrites

Koji Chono, Hiroshi Takagi, Shozo Koyama, Hideo Suzuki, Etsuro Ito

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

The present study was designed to elucidate the roles of dendritic voltage-gated K+ channels in Ca2+ influx mechanism of a rat Purkinje cell using a computer simulation program. First, we improved the channel descriptions and the maximum conductance in the Purkinje cell model to mimic both the kinetics of ion channels and the Ca2+ spikes, which had failed in previous studies. Our cell model is, therefore, much more authentic than those in previous studies. Second, synaptic inputs that mimic stimulation of parallel fibers and induce sub-threshold excitability were simultaneously applied to the spiny dendrites. As a result, transient Ca 2+ responses were observed in the stimulation points and they decreased with the faster decay rate in the cell model including high-threshold Ca2+-dependent K+ channels than in those excluding these channels. Third, when a single synaptic input was applied into a spiny dendrite, Ca2+-dependent K+ channels suppressed Ca2+ increases at stimulation and recording points. Finally, Ca 2+-dependent K+ channels were also found to suppress the time to peak Ca2+ values in the recording points. These results suggest that the opening of Ca2+-dependent K+ channels by Ca2+ influx through voltage-gated Ca2+ channels hyperpolarizes the membrane potentials and deactivates these Ca2+ channels in a negative feedback manner, resulting in local, weak Ca 2+ responses in spiny dendrites of Purkinje cells.

Original languageEnglish
Pages (from-to)115-127
Number of pages13
JournalJournal of Neuroscience Methods
Volume129
Issue number2
DOIs
Publication statusPublished - 2003 Oct 30
Externally publishedYes

Keywords

  • Ca channel
  • Dendrite
  • K channel
  • Multi-compartment model
  • Purkinje cell
  • Simulation

ASJC Scopus subject areas

  • Neuroscience(all)

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