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Background  Paclitaxel, which is widely used for the treatment of solid tumors, causes neuropathic pain via poorly understood mechanisms. Previously, we have demonstrated that lysophosphatidic acid (LPA) and its receptors (LPA 1  and LPA 3 ) are required for the initiation of peripheral nerve injury-induced neuropathic pain. The present study aimed to clarify whether LPA and its receptors could mediate paclitaxel-induced neuropathic pain.    Results  Intraperitoneal administration of paclitaxel triggered a marked increase in production of LPA species (18:1-, 16:0-, and 18:0-LPA) in the spinal dorsal horn. Also, we found significant activations of spinal cytosolic phospholipase A 2  and calcium-independent phospholipase A 2  after the paclitaxel treatment. The paclitaxel-induced LPA production was completely abolished not only by intrathecal pretreatment with neurokinin 1 (NK1) or  N -methyl- D -aspartate (NMDA) receptor antagonist, but also in LPA 1  receptor-deficient ( Lpar1  −/− ) and LPA 3  receptor-deficient ( Lpar3  −/− ) mice. In addition, the pharmacological blockade of NK1 or NMDA receptor prevented a reduction in the paw withdrawal threshold against mechanical stimulation after paclitaxel treatments. Importantly, the paclitaxel-induced mechanical allodynia was absent in  Lpar1  −/−  and  Lpar3  −/−  mice.    Conclusions  These results suggest that LPA 1  and LPA 3  receptors-mediated amplification of spinal LPA production is required for the development of paclitaxel-induced neuropathic pain.

Lysophosphatidic Acid and its Receptors LPA1 and LPA3 Mediate Paclitaxel-Induced Neuropathic Pain in Mice

Lysophosphatidic Acid and its Receptors LPA₁ and LPA₃ Mediate Paclitaxel-Induced Neuropathic Pain in Mice