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Updated: Mar 12, 2026

Assessment of Morphine-induced Hyperalgesia and Analgesic Tolerance in Mice Using Thermal and Mechanical Nociceptive Modalities
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Sustained Morphine Administration Induces TRPM8-Dependent Cold Hyperalgesia.

Kerui Gong1, Luc Jasmin1

  • 1Department of Oral and Maxillofacial Surgery, University of California San Francisco, San Francisco, California.

The Journal of Pain
|November 16, 2016
PubMed
Summary
This summary is machine-generated.

Chronic opioid use can cause cold sensitivity. This study reveals that morphine increases the TRPM8 channel, a key factor in opioid-induced cold hyperalgesia, which can be blocked by targeting TRPM8.

Keywords:
5°CCold receptorcold platementholpaw liftwhole cell recording

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Pain Research

Background:

  • Opioid-induced hyperalgesia is a common clinical issue.
  • Cold allodynia is a frequent complaint in patients on chronic opioid therapy.
  • The underlying molecular mechanisms of cold allodynia are not fully understood.

Purpose of the Study:

  • To investigate the role of the transient receptor potential melastatin 8 (TRPM8) channel in opioid-induced cold hyperalgesia.
  • To determine if chronic morphine administration affects TRPM8 expression and function.

Main Methods:

  • Chronic morphine administration in rats and mice.
  • Patch-clamp electrophysiology on sensory neurons.
  • Western blot analysis of dorsal root ganglia.
  • Pharmacological blockade of TRPM8 using RQ-00203078.
  • Assessment of cold hyperalgesia in TRPM8 knockout mice.

Main Results:

  • Chronic morphine administration led to an upregulation of TRPM8 channels in sensory neurons.
  • Selective TRPM8 antagonist RQ-00203078 reversed cold hyperalgesia in morphine-treated rats.
  • TRPM8 knockout mice did not develop cold hyperalgesia after chronic morphine treatment.
  • These findings contrast with acute morphine's effect of triggering TRPM8 internalization.

Conclusions:

  • The transient receptor potential melastatin 8 (TRPM8) channel is critically involved in the development of opioid-induced cold hyperalgesia.
  • Chronic morphine treatment upregulates TRPM8 channels, contributing to cold hypersensitivity.
  • Targeting TRPM8 presents a potential therapeutic strategy for managing opioid-induced cold allodynia.