Ryanodine Receptor-mediated Calcium Release Regulates Neuronal Excitability in Rat Spinal Substantia Gelatinosa Neurons
International Journal of Oral Biology
; : 211-216, 2015.
Article
in Ko
| WPRIM
| ID: wpr-42181
Responsible library:
WPRO
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.
Key words
Full text:
1
Index:
WPRIM
Main subject:
Potassium
/
Ryanodine
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Substantia Gelatinosa
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Tissue Donors
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Nitroprusside
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Calcium
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Charybdotoxin
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Thapsigargin
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Ryanodine Receptor Calcium Release Channel
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Endoplasmic Reticulum
Limits:
Animals
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Humans
Language:
Ko
Journal:
International Journal of Oral Biology
Year:
2015
Type:
Article