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Updated: Jun 27, 2025

Rapid Isolation of Dorsal Root Ganglion Macrophages
Published on: September 7, 2019
Macrophage/microglia-producing transient increase of platelet-activating factor is involved in neuropathic pain
Shota Yamamoto1,2, Tomomi Hashidate-Yoshida1, Yuki Yoshinari1,3
1Department of Lipid Life Science, National Center for Global Health and Medicine, Shinjuku-ku, Tokyo 162-8655, Japan.
Abstract:
Peripheral nerve injury (PNI) induces debilitating neuropathic pain symptoms, such as tactile allodynia. Accumulating evidence suggests that the expression levels of various transcripts and proteins are drastically changed after PNI. Recent lipidome analysis demonstrates increased levels of diverse lipids in chronic pain conditions. We show that PNI transiently increases platelet-activating factor (PAF) levels, a potent inflammatory phospholipid mediator, in the dorsal root ganglia (DRG) and spinal cord. We revealed that macrophage and microglia-specific PAF-producing enzyme LPLAT9/LPCAT2 knockout mice (Cx3cr1CreERT2;Lpcat2flox/flox) failed to develop mechanical allodynia and to increase PAF levels in the DRG and spinal cord after PNI. Moreover, we observed the suppression of PNI-induced PAF increase in the spinal cord of PAF receptor knockout mice, indicating a self-amplification loop of PAF production. In conclusion, macrophages and microglia enhance PAF production, contributing to PNI-induced neuropathic pain. Additionally, PAF-PAF receptor signaling is a potential target of neuropathic pain control.
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