Involvement of TRPV1 in Acute Inflammatory Pain Induced by Intraplantar Injection of Monosodium Iodoacetate in Rats

Objective: To investigate whether intraplantar injection of monosodium iodoacetate (MIA) in rats produces acute inflammatory pain and to explore whether the hyperalgesia is mediated by transient receptor potential vanilloid type 1 (TRPV1). Methods: Male Wistar rats were used in the study. MIA was injected intraplantarly into the sole of the left hindpaw of rats and 30 minutes later, the paw skin color, paw volume, paw temperature, and serum IL-1β level of rats were measured. MIA was injected intraplantarly into the sole of the left hindpaw of rats and the changes of thermal pain latency, mechanical pain threshold, and dynamic weight bearing were measured after injection for one hour. TRPV1 antagonist capsazepine and MIA were co-injected intraplantarly into the sole of the left hindpaw of rats, and the changes in thermal pain latency, mechanical pain threshold, and dynamic weight bearing were measured for one hour after MIA injection. MIA was injected intraplantarly into the sole of the left hindpaw of rats and 30 minutes later, TRPV1 agonist capsaicin was injected intraplantarly to record capsaicin-induced guarding behavior. Results: The paw skin became red, the paw was swollen, and the paw temperature increased for the injected paw and the IL-1β level in the serum was elevated at 30 minutes after intraplantar injection of MIA in rats. Intraplantar injection of MIA in rats reduced the thermal pain latency, mechanical pain threshold, and dynamic weight bearing. The hyperalgesia lasted for at least one hour and the effect was dose-dependent. Intraplantar co-injection of capsazepine and MIA reversed the thermal hyperalgesia, mechanical hyperalgesia, and spontaneous pain induced by MIA. Rats showed more guarding behaviors such as paw lifting and paw licking in response to intraplantar injection of capsaicin at 30 minutes after intraplantar injection of MIA. Conclusion: Acute inflammatory pain can be produced by intraplantar injection of MIA in rats, which leads to the establishment of a novel animal model of acute inflammatory pain. MIA-induced acute inflammatory pain may be due to TRPV1 upregulation.