4.4 Article

Pulsed Radiofrequency Decreases pERK and Affects Intracellular Ca2+ Influx, Cytosolic ATP Level, and Mitochondrial Membrane Potential in the Sensitized Dorsal Root Ganglion Neuron Induced by N-Methyl D-Aspartate

Journal

JOURNAL OF PAIN RESEARCH
Volume 16, Issue -, Pages 1697-1711

Publisher

DOVE MEDICAL PRESS LTD
DOI: 10.2147/JPR.S409658

Keywords

pulsed radiofrequency; neurons; sensitization; calcium; ATP; mitochondrial membrane potential; NMDA; NMDAR

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This study investigates the effects of pulsed radiofrequency (PRF) on central sensitization in chronic pain management. The findings suggest that PRF alleviates neuron sensitization by reducing pERK, modulating Ca2+ influx, increasing cytosolic ATP level, and decreasing Delta psi m.
Background: The molecular mechanism of pulsed radiofrequency (PRF) in chronic pain management is not fully understood. Chronic pain involves the activation of specific N-Methyl D-Aspartate receptors (NMDAR) to induce central sensitization. This study aims to determine the effect of PRF on central sensitization biomarker phosphorylated extracellular signal-regulated kinase (pERK), Ca2+ influx, cytosolic ATP level, and mitochondrial membrane potential (Delta psi m) of the sensitized dorsal root ganglion (DRG) neuron following NMDAR activation. Methods: This study is a true experimental in-vitro study on a sensitized DRG neuron induced with 80 mu M NMDA. There are six treatment groups including control, NMDA 80 mu M, Ketamine 100 mu M, PRF 2Hz, NMDA 80 mu M + PRF 2 Hz, and NMDA 80 mu M + PRF 2 Hz + ketamine 100 mu M. We use PRF 2 Hz 20 ms for 360 seconds. Statistical analysis was performed using the One-Way ANOVA and the Pearson correlation test with alpha=5%. Results: In the sensitized DRG neuron, there is a significant elevation of pERK. There is a strong correlation between Ca2+, cytosolic ATP level, and Delta psi m with pERK intensity (p<0.05). PRF treatment decreases pERK intensity from 108.48 +/- 16.95 AU to 38.57 +/- 5.20 AU (p<0.05). PRF exposure to sensitized neurons also exhibits a Ca2+ influx, but still lower than in the unexposed neuron. PRF exposure in sensitized neurons has a higher cytosolic ATP level (0.0458 +/- 0.0010 mM) than in the unexposed sensitized neuron (0.0198 +/- 0.0004 mM) (p<0.05). PRF also decreases Delta psi m in the sensitized neuron from 109.24 +/- 6.43 AU to 33.21 +/- 1.769 AU (p<0.05). Conclusion: PRF mechanisms related to DRG neuron sensitization are by decreasing pERK, altering Ca2+ influx, increasing cytosolic ATP level, and decreasing Delta psi m which is associated with neuron sensitization following NMDAR activation.

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