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Related Experiment Video

Updated: May 30, 2026

Ex Vivo Release of Calcitonin Gene-Related Peptide from the Trigeminovascular System in Rodents
08:39

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Published on: May 16, 2022

Platelet-activating factor and pain.

Makoto Tsuda1, Hidetoshi Tozaki-Saitoh, Kazuhide Inoue

  • 1Department of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka 812–8582, Japan.

Biological & Pharmaceutical Bulletin
|August 2, 2011
PubMed
Summary
This summary is machine-generated.

Platelet-activating factor (PAF) plays a role in chronic pain signaling. Blocking the PAF receptor (PAFR) may offer a new therapeutic strategy for neuropathic pain.

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Determining heat and mechanical pain threshold in inflamed skin of human subjects
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Determining heat and mechanical pain threshold in inflamed skin of human subjects

Published on: January 14, 2009

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Last Updated: May 30, 2026

Ex Vivo Release of Calcitonin Gene-Related Peptide from the Trigeminovascular System in Rodents
08:39

Ex Vivo Release of Calcitonin Gene-Related Peptide from the Trigeminovascular System in Rodents

Published on: May 16, 2022

Determining heat and mechanical pain threshold in inflamed skin of human subjects
13:21

Determining heat and mechanical pain threshold in inflamed skin of human subjects

Published on: January 14, 2009

Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Platelet-activating factor (PAF) is a phospholipid mediator involved in cellular functions in peripheral tissues and the nervous system.
  • PAF signaling, particularly through its receptor (PAFR), has been implicated in pain signaling, especially following tissue injury.
  • While not involved in acute physiological pain, the PAF/PAFR system is increasingly recognized for its role in pathological pain states.

Purpose of the Study:

  • To investigate the role of the Platelet-activating factor receptor (PAFR) in the development and maintenance of neuropathic pain.
  • To explore the potential of targeting the PAF/PAFR system as a therapeutic strategy for chronic pain conditions.

Main Methods:

  • Utilized pharmacological antagonists and genetic knockout models (PAFR-deficient mice) to study PAFR function.
  • Examined the expression of PAFRs in dorsal root ganglion (DRG) neurons following nerve injury.
  • Assessed the production of pro-inflammatory cytokines, including tumor necrosis factor α (TNFα) and interleukin-1β (IL-1β), in the DRG.

Main Results:

  • Nerve injury leads to upregulation of PAFRs in DRG neurons.
  • PAFR signaling is crucial for the production of TNFα and IL-1β in the DRG.
  • Blocking PAFR function significantly impacts the development and maintenance of neuropathic pain.

Conclusions:

  • The PAF/PAFR system plays a critical role in neuropathic pain pathogenesis, particularly through cytokine production in the DRG.
  • Targeting PAFRs represents a promising therapeutic avenue for managing neuropathic pain, a condition with limited effective treatments.