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Attenuated cold sensitivity in TRPM8 null mice.

Raymond W Colburn1, Mary Lou Lubin, Dennis J Stone

  • 1Analgesics Team, East Coast Research and Early Development, Johnson and Johnson Pharmaceutical Research and Development, L.L.C., Spring House, PA 19477-0776, USA.

Neuron
|May 8, 2007
PubMed
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The Transient Receptor Potential melastatin 8 (TRPM8) channel is crucial for sensing cold and menthol. TRPM8-deficient mice show impaired cold sensation and reduced responses to cold-induced pain, highlighting its role in thermosensation.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Sensory Physiology

Background:

  • Thermosensation relies on transducer molecules, including the Transient Receptor Potential (TRP) superfamily.
  • TRPM8 (CMR1) is a TRP channel activated by cold and chemicals in vitro.
  • The in vivo roles of TRPM8 in cold sensation and pain remain unclear.

Purpose of the Study:

  • To investigate the in vivo function of TRPM8 in cold thermosensation and pain.
  • To elucidate the role of TRPM8 in sensory neurons and behavioral responses.

Main Methods:

  • Utilized TRPM8 null mice and compared them to wild-type (WT) controls.
  • Assessed TRPM8 mRNA and protein levels in sensory neurons.
  • Measured neuronal responses to cold (18°C) and menthol (100 µM).

Related Experiment Videos

  • Evaluated behavioral responses, including icilin-induced jumping and acetone cooling sensitivity.

    • Main Results:

    • TRPM8 null mice exhibited significantly reduced TRPM8 mRNA and protein.
    • A marked decrease in cold- and menthol-responsive sensory neurons was observed in TRPM8 null mice.
    • TRPM8 null mice showed impaired cold sensation and reduced responses to icilin and acetone cooling.

    Conclusions:

    • TRPM8 plays a significant role in cold thermosensation and certain types of cold-induced pain.
    • These findings suggest TRPM8's importance in mediating physiological responses to cold stimuli in vivo.