Effect of nitric oxide on the somatic membrane of rat DRG neurons.
- Author:
Hong-Ju CHENG
1
;
Ke-Tao MA
;
Lei ZHAO
;
Li LI
;
Ying-Ying CAO
;
Jun-Qiang SI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Female; Ganglia, Spinal; physiology; Male; Membrane Potentials; physiology; Neurons; physiology; Nitric Oxide; pharmacology; Nitroprusside; pharmacology; Pain; physiopathology; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Applied Physiology 2009;25(4):535-538
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo observe the role of nitric oxide in dorsal root ganglion (DRG) neurons and its related ionic mechanisms, and explore the function of NO in pain transmission process.
METHODSIn freshly isolated rat DRG samples, using intracellular recording technique, we perfused sodium nitroprusside (NO donor) to observe the role of NO in DRG neurons.
RESULTSIn 77.45% of the bath cells, application of sodium nitroprusside (10 -100 mmol/L) induced concentration-dependent membrane hyperpolarization (79/102), and remaining neurons had no response. The membrane conductance increased from control value of (21.06 +/- 1.94) nS to (23.08 +/- 0.92) nS during sodium nitroprusside induced hyperpolarization. L-NAME (1 mmol/L), CdCl2 (0.1 mmol/L) and non-sodium BSS failed to change the amplitude of sodium nitroprusside induced hyperpolarization. When BSS containing 10 mmol/L TEA was used, sodium nitroprusside induced hyperpolarization was obviously inhibited.
CONCLUSIONSodium nitroprusside could cause concentration-dependent hyperpolarization in DRG neurons by activating K+ channels.
