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PPAR&ggr; Agonists Attenuate Trigeminal Neuropathic Pain

Objectives: The aim of this study is to investigate the role of peroxisome proliferator-activated receptor-gamma isoform (PPAR&ggr;), in trigeminal neuropathic pain utilizing a novel mouse trigeminal inflammatory compression (TIC) injury model. Results: The study determined that the PPAR&ggr; nuclear receptor plays a significant role in trigeminal nociception transmission, evidenced by: 1) Intense PPAR&ggr; immunoreactivity is expressed 3 weeks after TIC nerve injury in the spinal trigeminal caudalis, the termination site of trigeminal nociceptive nerve fibers. 2) Systemic administration of a PPAR&ggr; agonist, pioglitazone (PIO), attenuates whisker pad mechanical allodynia at doses of 300 mg/kg i.p. and 600 mg/kg p.o. 3) Administration of a PPAR&ggr; antagonist, GW9662 (30 mg/kg i.p.), prior to providing the optimal dose of PIO (300 mg/kg i.p.) blocked the analgesic effect of PIO. Discussion: This is the first study localizing PPAR&ggr; immunoreactivity throughout the brainstem trigeminal sensory spinal nucleus (spV) and its increase three weeks after TIC nerve injury. This is also the first study to demonstrate that activation of PPAR&ggr; attenuates trigeminal hypersensitivity in the mouse TIC nerve injury model. The findings presented here suggest the possibility of utilizing the FDA approved diabetic treatment drug, PIO, as a new therapeutic that targets PPAR&ggr; for treatment of patients suffering from orofacial neuropathic pain.