Int J Oral Biol.  2015 Dec;40(4):211-216. 10.11620/IJOB.2015.40.4.211.

Ryanodine Receptor-mediated Calcium Release Regulates Neuronal Excitability in Rat Spinal Substantia Gelatinosa Neurons

• Park A
• Chun SW

• KMID: 2133226
• DOI: http://doi.org/10.11620/IJOB.2015.40.4.211

Abstract

Nitric Oxide (NO) is an important signaling molecule in the nociceptive process. Our previous study suggested that high concentrations of sodium nitroprusside (SNP), a NO donor, induce a membrane hyperpolarization and outward current through large conductances calcium-activated potassium (BKca) channels in substantia gelatinosa (SG) neurons. In this study, patch clamp recording in spinal slices was used to investigate the sources of Ca2+ that induces Ca2+-activated potassium currents. Application of SNP induced a membrane hyperpolarization, which was significantly inhibited by hemoglobin and 2-(4-carboxyphenyl) -4,4,5,5- tetramethylimidazoline-1-oxyl-3-oxide potassium salt (c-PTIO), NO scavengers. SNP-induced hyperpolarization was decreased in the presence of charybdotoxin, a selective BKCa channel blocker. In addition, SNP-induced response was significantly blocked by pretreatment of thapsigargin which can remove Ca2+ in endoplasmic reticulum, and decreased by pretreatment of dentrolene, a ryanodine receptors (RyR) blocker. These data suggested that NO induces a membrane hyperpolarization through BKca channels, which are activated by intracellular Ca2+ increase via activation of RyR of Ca2+ stores.

Keyword

substantia gelatinosa neuron; nitric oxide; calcium release; ryanodine receptor; patch clamp

MeSH Terms

Animals
Calcium*
Charybdotoxin
Endoplasmic Reticulum
Humans
Membranes
Neurons*
Nitric Oxide
Nitroprusside
Potassium
Rats*
Ryanodine Receptor Calcium Release Channel
Ryanodine*
Substantia Gelatinosa*
Thapsigargin
Tissue Donors
Calcium
Charybdotoxin
Nitric Oxide
Nitroprusside
Potassium
Ryanodine
Ryanodine Receptor Calcium Release Channel
Thapsigargin