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Mice lacking NKCC1 have normal olfactory sensitivity.

David W Smith1, Sokunthirith Thach, Erika L Marshall

  • 1Department of Psychology, University of Florida, Gainesville, FL 32611, United States.

Physiology & Behavior
|August 28, 2007
PubMed
Summary
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The Na(+)+K(+)+2Cl(-) cotransporter (NKCC1) is crucial for chloride accumulation in isolated olfactory neurons. However, mice lacking NKCC1 show normal olfactory sensitivity, indicating it

Area of Science:

  • Neuroscience
  • Olfactory Receptor Neuron Physiology
  • Ion Transport Mechanisms

Background:

  • Olfactory receptor neurons (ORNs) utilize chloride efflux for odorant response, necessitating intracellular chloride accumulation against electrochemical gradients.
  • The Na(+)+K(+)+2Cl(-) cotransporter 1 (NKCC1) is identified as essential for chloride accumulation in isolated ORNs.
  • A discrepancy exists between isolated neuron findings and intact olfactory epithelium responses in NKCC1 knockout models.

Purpose of the Study:

  • To investigate the necessity of NKCC1 for normal olfactory sensitivity in a whole-animal model.
  • To compare olfactory detection thresholds between NKCC1 knockout mice and wild-type littermates.

Main Methods:

  • Utilized knockout (KO) mice with a null mutation for NKCC1 and their wild-type (WT) littermates.

Related Experiment Videos

  • Employed operant behavioral techniques and a commercial liquid-dilution olfactometer to assess olfactory sensitivity.
  • Measured behavioral detection thresholds for simple odorants: cineole, 1-heptanol, and 1-propanol.

    • Main Results:

    • No systematic differences in behavioral olfactory detection thresholds were observed between NKCC1 KO and WT mice.
    • This lack of difference persisted across various stimulus conditions tested.
    • The findings challenge the essential role of NKCC1 in mediating olfactory responses in the intact olfactory epithelium.

    Conclusions:

    • The Na(+)+K(+)+2Cl(-) cotransporter 1 (NKCC1) is not required for normal olfactory sensitivity in mice.
    • Alternative mechanisms likely compensate for NKCC1's absence in maintaining olfactory function within the intact epithelium.
    • Further research is needed to elucidate compensatory ion transport pathways in ORNs.