Rapid inhibition of ATP-induced currents by dexamethasone in rat dorsal root ganglion neurons
- VernacularTitle:地塞米松对大鼠背根神经节细胞ATP激活电流的快速抑制作用
- Author:
Xiaohong LIU
;
Junwei ZENG
;
Huaizhen RUAN
- Publication Type:Journal Article
- Keywords:
dexamethasone;
ganglia, spinal;
adenosine triphosphate;
patch-clamp techniques
- From:
Medical Journal of Chinese People's Liberation Army
1983;0(05):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective Glucocorticoid hormone may nongenomically affect cell functions in addition to its classic effects on gene expression. The purpose of present study was to explore whether dexamethasone, a synthetical glucocorticoid hormone, has a rapid nongenomic effect on ATP-induced currents in rat dorsal root ganglion (DRG) neurons and the related signal transduction pathway. Methods The effects of dexamethasone on ATP-induced currents were studied on cultured DRG neurons using patch clamp technique. Results Three types of currents (transient, sustained and biphasic) were evoked by ATP (100 ?mol/L) in cultured DRG neurons. When DRG neurons were pretreated with dexamethasone (0.01-10?mol/L) for 30s, inhibition of the transient current and the transient component of the biphasic current evoked by ATP in DRG neurons was observed. The inhibitory effect of dexamethasone was dose-dependent. However, dexamethasone did not seem to affect the sustained current and the sustained component of the biphasic current induced by ATP. The inhibitory effect of dexamethasone on ATP-induced currents was blocked by glucocorticoid receptor antagonist RU38486 (10?mol/L) and protein kinase A inhibitor H-89 (10?mol/L), but not by G protein inhibitor GDP-?-S (0.2mmol/L) and protein kinase C inhibitor chelerythrine chloride (10?mol/L). Conclusions Dexamethasone can selectively inhibit the transient current mediated by P2X3 receptors in DRG neurons. The inhibitory effect of dexamethasone might be mediated by glucocorticoid receptor through activating PKA signal pathway. These results suggest that glucocorticoid hormone might participate in the control of pain by modulating the actions of extracellular ATP in sensory neurons.
