Change of SNS/PN3 Na + channel expression in dorsal root ganglion neurons in the chronic constriction injury model of neuropathic pain
- VernacularTitle:坐骨神经压迫性损伤大鼠背根神经节SNS/PN3钠通道表达的变化
- Author:
Wei WEI
;
Haosheng BI
;
Yang LI
- Publication Type:Journal Article
- Keywords:
Sodium channels;
Nerve compression syndromes;
Sciatic nerve;
Ganglia, spinal
- From:
Chinese Journal of Anesthesiology
1994;0(06):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the changes in small-diameter sensory neuron (SNS)/ peripheral nerve type 3(PN3) Na+ channel transcript and in tetrodotoxin-resistant (TTX-R) Na+ current in dorsal root ganglion (DRG) neurons in a chronic constriction injury (CCI) model of neuropathic pain. Methods Eighteen rats were divided into 6 groups of 3 animals each. Chronic constriction injury model was established after Dib-Hajj et al. Pain threshold was significantly lowered after CCI as compared with that in control group. The animals were deeply anesthetized and rapidly decapitated 14 days after surgery. The L4-5 DRG of the operated side was removed and crushed and total RNA was extracted with trizol reagent. The DRG of the contralateral side was used as control. The change in SNS/PN3 Na + channel expression was determined by semi-reverse transcriptase-PCR. The DRG neurons were isolated enzymatically and the change in voltage-gated TTX-R Na+ current was recorded using whole-cell patch clamp technique. Results Sensory neuron specific TTX-R Na+ channel transcript SNS/PN3 was down-regulated by 60% 14 days after CCI as compared with that in control group. TTX-R Na+ current density was significantly reduced but its activation and steady state inactivation were unchanged. Conclusions Na+ channel SNS/PN3 is involved in the hyperextability of the primary sensory neurons after CCI.
