Background and Objective: Radiofrequency ablation (RFA) is a safe and less invasive technique that uses an electric current to damage nerve tissue to stop it from sending pain signals. This study was aimed to determine the molecular mechanism of neuropathologic damage induced by RFA at different temperatures.Methods: A total of 36 Sprague Dawley rats were used as model with neuropathological injury. These rats were divided into six groups based on the temperature stimulation at 42°C, 47°C, 52°C, 57°C, 62°C, and 67°C. Conduction time, distance, and velocity were recorded after thermal injury. Hematoxylin and eosin staining was used to observe the histopathological changes of sciatic nerve. Neural ion channel proteins such as sodium voltage-gated channel alpha subunit 9 (SCN9A), sodium channel B3 subunit (SCN3B) and neurofascin (NFASC) expression in sciatic nerve tissue were detected detected by Western Blot.Results: Nerve conduction velocity (NCV) gradually decreased with the increase in temperature and neuronal damage was seen at 67°C. H&E staining showed increased degeneration of neurons with an increase in temperature from 47°C to 67°C. SCN9A and SCN3B expression at 57°C, 62°C, and 67°C was much higher; however, NFASC expression was lower at same temperatures.Conclusion: Neuropathological damage caused by RFA at different temperatures shows positive correlation with NCV. Heat transfer injury affects the expression of SCN9A, SCN3B, and NFASC in sciatic nerve tissue.
