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Apoptotic surface delivery of K+ channels

S K Pal1, K Takimoto, E Aizenman

  • 1Department of Neurobiology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15217, USA.

Cell Death and Differentiation
|November 8, 2005
PubMed

Insights

Apoptosis in cortical neurons involves increased Kv2.1 channel activity. New Kv2.1 channels are inserted into the cell membrane during apoptosis, leading to potassium (K+) efflux and cell death.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Apoptosis, or programmed cell death, in cortical neurons is linked to potassium (K+) efflux.
  • Kv2.1 channels play a critical role in mediating this K+ efflux during neuronal apoptosis.

Purpose of the Study:

  • To investigate the mechanism behind the surge in Kv2.1 channel activity during apoptosis.
  • To determine if de novo channel insertion into the plasma membrane contributes to apoptotic K+ current.

Main Methods:

  • Utilized a cysteine-containing Kv2.1 mutant and a thiol-reactive covalent inhibitor.
  • Employed biotinylation assays to assess cell surface protein levels.
  • Investigated the role of SNARE proteins using botulinum neurotoxins targeting syntaxin and SNAP-25.

Main Results:

  • Demonstrated that increased K+ current during apoptosis results from the insertion of new Kv2.1 channels into the plasma membrane.
  • Biotinylation experiments confirmed increased Kv2.1 protein at the cell surface after apoptotic stimuli.
  • Disruption of SNARE proteins (syntaxin, SNAP-25) inhibited the surface upregulation of Kv2.1 channels.

Conclusions:

  • The surge in K+ current during cortical neuron apoptosis is caused by the trafficking and insertion of functional Kv2.1 channels into the plasma membrane.
  • SNARE proteins are implicated in supporting the delivery of Kv2.1 channels to the cell surface during apoptosis.

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