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

© 2023 Laksono et al..

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 (Δψm) 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 µM NMDA. There are six treatment groups including control, NMDA 80 µM, Ketamine 100 µM, PRF 2Hz, NMDA 80 µM + PRF 2 Hz, and NMDA 80 µM + PRF 2 Hz + ketamine 100 µM. 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 α=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 Δψm 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 Δψm 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 Δψm which is associated with neuron sensitization following NMDAR activation.

Errataetall:

ErratumIn: J Pain Res. 2023 Jun 20;16:2131-2132. - PMID 37361427

Medienart:

E-Artikel

Erscheinungsjahr:

2023

Erschienen:

2023

Enthalten in:

Zur Gesamtaufnahme - volume:16

Enthalten in:

Journal of pain research - 16(2023) vom: 25., Seite 1697-1711

Sprache:

Englisch

Beteiligte Personen:

Laksono, Ristiawan Muji [VerfasserIn]
Kalim, Handono [VerfasserIn]
Rohman, Mohammad Saifur [VerfasserIn]
Widodo, Nashi [VerfasserIn]
Ahmad, Muhammad Ramli [VerfasserIn]
Halim, Willy [VerfasserIn]

Links:

Volltext

Themen:

ATP
Calcium
Journal Article
Mitochondrial membrane potential
NMDA
NMDAR
Neurons
Pulsed radiofrequency
Sensitization

Anmerkungen:

Date Revised 26.06.2023

published: Electronic-eCollection

ErratumIn: J Pain Res. 2023 Jun 20;16:2131-2132. - PMID 37361427

Citation Status PubMed-not-MEDLINE

doi:

10.2147/JPR.S409658

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM357542746