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Related Experiment Video

Updated: Sep 1, 2025

Cheek Injection Model for Simultaneous Measurement of Pain and Itch-related Behaviors
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An LPAR -antagonist that reduces nociception and increases pruriception.

Jacqueline Langedijk1, Erika Ivanna Araya2, Amanda Ribeiro Barroso2

  • 1Amsterdam University Medical Centers (UMC), Tytgat Institute for Liver and Intestinal Research, University of Amsterdam, Research Institute Amsterdam Gastroenterology, Endocrinology and Metabolism (AG&M), Amsterdam, Netherlands.

Frontiers in Pain Research (Lausanne, Switzerland)
|August 12, 2022
PubMed
Summary

Compound 3 (cpd3) reduces pain signaling in mice but unexpectedly causes scratching, potentially by activating TRPA1 and other itch receptors. Further screening is needed for pain relief drugs.

Keywords:
LPAR5TRPA1 (transient receptor potential A1)compound 3hyperalgesiainflammatory painitch (pruritus)nociception

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Molecular Biology

Background:

  • Lysophosphatidic acid receptor 5 (LPAR5) is crucial for pain and itch signaling.
  • Compound 3 (cpd3) is an LPAR5 antagonist investigated for its effects on these pathways.

Purpose of the Study:

  • To evaluate the in vitro and in vivo effects of cpd3 on pain and itch signaling.
  • To determine the role of TRPA1 in cpd3-induced effects.

Main Methods:

  • Nociceptive behavior was induced by formalin, carrageenan, or prostaglandin E2 (PGE2) in mice.
  • Scratch activity was measured in wild-type, phospholipase A2-overexpressing, and TRPA1-deficient mice.
  • In vitro studies involved measuring intracellular calcium release in HMC-1 and HEK-TRPA1 cells.

Main Results:

  • Cpd3 significantly reduced nociceptive behavior induced by various stimuli.
  • Unexpectedly, cpd3 administration increased scratch activity in mice.
  • In vitro, cpd3 triggered calcium release in HEK-TRPA1 cells, which was blocked by a TRPA1 antagonist, but scratch activity in TRPA1-deficient mice was not reduced.

Conclusions:

  • Cpd3 exhibits in vivo antinociceptive effects but also induces scratching, likely via TRPA1 and other pruriceptors.
  • These findings highlight the necessity of screening antinociceptive drug candidates for potential activity on pruriceptors.