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Updated: Mar 22, 2026
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A Simple and Inexpensive Method for Determining Cold Sensitivity and Adaptation in Mice
Published on: March 17, 2015
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Phospholipase C δ4 regulates cold sensitivity in mice
Yevgen Yudin1, Brianna Lutz2, Yuan-Xiang Tao1,2
1Department of Pharmacology, Physiology and Neuroscience, Rutgers, New Jersey Medical School, Newark, NJ, USA.
The Journal of Physiology
|April 11, 2016
Summary
Phospholipase C delta 4 (PLCδ4) regulates the cold and menthol sensor TRPM8 channels in vivo. PLCδ4 deficiency enhances cold sensitivity in mice by increasing TRPM8 channel activity.
Area of Science:
- Neuroscience
- Molecular Biology
- Physiology
Background:
- Transient receptor potential melastatin 8 (TRPM8) channels sense cold and menthol.
- Phospholipase C (PLC) is implicated in TRPM8 regulation, but the specific isoform and in vivo relevance are unclear.
Purpose of the Study:
- Identify the key PLC isoform regulating TRPM8 channels in vivo.
- Investigate the role of PLCδ4 in TRPM8-mediated cold sensation.
Main Methods:
- Utilized PLCδ4 knockout (KO) mice and wild-type (WT) littermates.
- Electrophysiological recordings from dorsal root ganglion (DRG) neurons.
- Behavioral assays measuring responses to cold, heat, and mechanical stimuli.
Main Results:
- PLCδ4 deficiency in small DRG neurons led to larger TRPM8-mediated currents and increased action potential firing.
- PLCδ4 KO mice exhibited heightened behavioral sensitivity to evaporative cooling.
- TRPM8 antagonist administration reduced cold-evoked responses, particularly in PLCδ4 KO mice.
Conclusions:
- PLCδ4 is the critical PLC isoform regulating TRPM8 channel activity in vivo.
- PLCδ4 plays a significant role in modulating cold sensitivity through TRPM8 channels.
- Targeting PLCδ4 may offer new strategies for managing cold-related sensory disorders.
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