Effects of NaOCl on the Intracellular Calcium Concentration in Rat Dorsal Root Ganglion Neurons.
- Author:
Hae In LEE
1
;
Sang Woo CHUN
Author Information
1. Department of Oral Physiology, College of Dentistry, Institute of Wonkwang Biomaterial and Implant, Wonkwang University, Iksan 570-749, Korea. physio1@wonkwang.ac.kr
- Publication Type:Original Article
- Keywords:
reactive oxygen species;
intracellular calcium concentration;
dorsal root ganglion;
transient receptor potential channel
- MeSH:
Animals;
Calcium;
Capsaicin;
Diagnosis-Related Groups;
Dissociative Disorders;
Extracellular Fluid;
Ganglia, Spinal;
Humans;
Neurons;
Rats;
Reactive Oxygen Species;
Ruthenium Red;
Sensation;
Sensory Receptor Cells;
Spinal Nerve Roots;
Thapsigargin;
Thermolysin;
Tissue Donors
- From:International Journal of Oral Biology
2010;35(3):129-135
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Recent studies have implicated reactive oxygen species (ROS) as determinants of the pathological pain caused by the activation of peripheral neurons. It has not been elucidated, however, how ROS activate the primary sensory neurons in the pain pathway. In this study, calcium imaging was performed to investigate the effects of NaOCl, a ROS donor, on the intracellular calcium concentration ([Ca2+]i) in acutely dissociated dorsal root ganglion (DRG) neurons. DRG was sequentially treated with 0.2 mg/ml of both protease and thermolysin, and single neurons were then obtained by mechanical dissociation. The administration of NaOCl then caused a reversible increase in the [Ca2+]i, which was inhibited by pretreatment with phenyl-N-tert-buthylnitrone (PBN) and isoascorbate, both ROS scavengers. The NaOCl-induced [Ca2+]i increase was suppressed both in a calcium free solution and after depletion of the intracellular Ca2+ pool by thapsigargin. Additionally, this increase was predominantly blocked by pretreatment with the transient receptor potential (TRP) antagonists, ruthenium red (50 microM) and capsazepine (10 microM). Collectively, these results suggest that an increase in the intracellular calcium concentration is produced from both extracellular fluid and the intracellular calcium store, and that TRP might be involved in the sensation of pain induced by ROS.
