Role of spinal LPCAT2, an inducible PAR synthesis enzyme on development and maintenance of painful peripheral neuropathy models in mice

Pain in peripheral neuropathies is produced by damage or illness affecting nerve fibers themselves, and often resistant to current analgesics. We have previously suggested that PAF may be a mediator of neuropathic pain. PAF injection into the mouse spinal cord caused thermal hyperalgesia and tactile allodynia, which were at least in part mediated by spinal dysfunction of glycine receptor a3 (GlyRa3) and were blocked by PAF receptor antagonists [Morita et al., Pain 111:351-359,2004; Pain 138: 525-536,2008]. Subsequent studies showed PAF receptor blockade reduced pain behaviors elicited in nerve injury models [Okubo et al., Mol Pain 8(8):doi:10.1186,2012; Motoyama et al., Eur J Pain 17(8):1156-1167,2013; Morita et al., PlosOne 9(3):e91746,2014].