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Activation of Ca2+--calmodulin kinase II induces desensitization by background light in dogfish retinal 'on' bipolar

R A Shiells1, G Falk

  • 1Biophysics Unit, Physiology Department, University College London, Gower Street, London WC1E 6BT, UK.

The Journal of Physiology
|October 18, 2000
PubMed

Insights

Calcium-calmodulin kinase II (CaMKII) inhibition prevents desensitization in retinal "on" bipolar cells. This suggests CaMKII phosphorylation of cGMP-activated channels underlies light-induced desensitization.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Phototransduction

Background:

  • Retinal "on" bipolar cells utilize metabotropic glutamate receptor 6 (mGluR6) for signal transduction.
  • These cells exhibit high synaptic amplification of rod signals in dark conditions.
  • Desensitization of "on" bipolar cells is triggered by intracellular calcium (Ca2+) increases.

Purpose of the Study:

  • To investigate the molecular mechanisms of desensitization in retinal "on" bipolar cells.
  • To determine the role of Ca2+-calmodulin kinase II (CaMKII) in this desensitization process.

Main Methods:

  • Whole-cell current recordings from voltage-clamped "on" bipolar cells in dogfish retinal slices.
  • Application of CaMKII inhibitor peptides via patch pipette.
  • Stimulation with dim background light and controlled Ca2+ levels.

Main Results:

  • CaMKII inhibition blocked desensitization induced by dim light and elevated intracellular Ca2+.
  • Inhibition of CaMKII enhanced the flash sensitivity of "on" bipolar cells.
  • Phosphorylation targets of CaMKII were identified as the cGMP-activated channels.

Conclusions:

  • CaMKII-mediated phosphorylation of cGMP-activated channels reduces their cGMP sensitivity, leading to desensitization.
  • This phosphorylation contributes to a voltage-dependent decrease in channel conductance.
  • Protein kinase C (PKC) activation did not induce desensitization, excluding its role in this specific pathway.

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