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A selective PMCA inhibitor does not prolong the electroolfactogram in mouse.

Edwin R Griff1, Nancy K Kleene, Steven J Kleene

  • 1Department of Biological Sciences, University of Cincinnati, Cincinnati, Ohio, United States of America.

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|May 23, 2012
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Summary

Calcium removal is crucial for ending odor responses in olfactory neurons. This study found that while sodium-calcium exchange is important, plasma membrane calcium-ATPase (PMCA) does not significantly contribute to this calcium clearance.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Sensory Physiology

Background:

  • Calcium ions (Ca2+) accumulate in olfactory receptor neuron cilia during odor transduction.
  • Efficient Ca2+ removal is essential for terminating olfactory responses.
  • Both Na+/Ca2+ exchange and PMCA were previously suggested to mediate Ca2+ removal.

Purpose of the Study:

  • To investigate the specific contribution of PMCA to Ca2+ removal during olfactory response termination.
  • To differentiate the roles of Na+/Ca2+ exchange and PMCA in clearing intracellular Ca2+.

Main Methods:

  • Measurements of odor-induced field potential termination time course in intact mouse olfactory epithelium.
  • Experimental manipulation using Li+ to inhibit Na+/Ca2+ exchange.
  • Application of a specific PMCA inhibitor, caloxin 1b1.

Main Results:

  • Inhibition of Na+/Ca2+ exchange by replacing Na+ with Li+ significantly prolonged response termination, as anticipated.
  • Treatment with the PMCA inhibitor caloxin 1b1 did not result in a significant alteration of the response termination time course.
  • These findings indicate that PMCA activity is not a major factor in rapid Ca2+ clearance.

Conclusions:

  • Under the tested experimental conditions, PMCA does not play a detectable role in the termination of olfactory responses.
  • Na+/Ca2+ exchange appears to be the primary mechanism for Ca2+ extrusion in this context.
  • Further research may be needed to fully elucidate the complex mechanisms of calcium homeostasis in olfactory neurons.