Involvement of plasma membrane-located calmodulin in the response decay of cyclic nucleotide-gated cation channel of cultured carrot cells

FEBS Lett. 1994 Mar 7;340(3):193-6. doi: 10.1016/0014-5793(94)80136-3.

Abstract

Increase in cytoplasmic cyclic AMP concentration stimulates Ca2+ influx through the cyclic AMP-gated cation channel in the plasma membrane of cultured carrot cells. However, the Ca2+ current terminated after a few minutes even in the presence of high concentrations of cyclic AMP indicating that hydrolysis of the nucleotide is not responsible for stop of the Ca2+ influx. Cyclic AMP evoked discharge of Ca2+ from inside-out sealed vesicles of carrot plasma membrane, and it was strongly inhibited when the suspension of the vesicles was supplemented with 1 microM of free Ca2+, while Ca2+ lower than 0.1 microM did not affect the Ca(2+)-release. The Ca2+ flux across plasma membrane was restored from this Ca(2+)-induced inhibition by the addition of calmodulin inhibitors or anti-calmodulin. These results suggest that Ca2+ influx initiated by the increase in intracellular cAMP in cultured carrot cells is terminated when the cytosolic Ca2+ concentration reaches the excitatory level in the cells, and calmodulin located in the plasma membrane plays an important role in the response decay of the cyclic nucleotide-gated Ca2+ channel.

MeSH terms

  • Biological Transport
  • Calcium Channels / drug effects
  • Calcium Channels / metabolism*
  • Calmodulin / antagonists & inhibitors
  • Calmodulin / metabolism*
  • Cell Membrane / drug effects
  • Cell Membrane / metabolism
  • Cells, Cultured
  • Cyclic AMP / metabolism*
  • Ion Channel Gating*
  • Sulfonamides / pharmacology
  • Trifluoperazine / pharmacology
  • Vegetables

Substances

  • Calcium Channels
  • Calmodulin
  • Sulfonamides
  • Trifluoperazine
  • W 7
  • Cyclic AMP