Prostaglandin inhibitor indomethacin inhibits afferent activities of Adelta and C units in the saphenous nerve of diabetic hyperalgesic rats.
- Author:
Jian LIU
1
;
Qiao-Jun ZHANG
;
Bei-Chuan GUO
;
Dong-Yuan CAO
;
Ke-Mo WANG
Author Information
1. Department of Physiology, School of Medicine, Xi'an Jiao Tong University, Xi'an, China. physi-x@mail.xjtu.edu.cn
- Publication Type:Journal Article
- MeSH:
Afferent Pathways;
drug effects;
physiopathology;
Animals;
Diabetes Mellitus, Experimental;
physiopathology;
Femoral Nerve;
drug effects;
physiopathology;
Hyperalgesia;
physiopathology;
Indomethacin;
pharmacology;
Male;
Pain Threshold;
drug effects;
Prostaglandin Antagonists;
pharmacology;
Rats;
Rats, Sprague-Dawley
- From:
Acta Physiologica Sinica
2002;54(5):379-384
- CountryChina
- Language:Chinese
-
Abstract:
The effects of a non-selective inhibitor of cyclo-oxygenase (COX) indomethacin, and exogenous prostaglandin E(2) (PGE(2)) on A(delta) units and C units in the saphenous nerve of diabetic hyperalgesic rats were studied. The results showed that the conduction velocity of A(delta) units and C units and their mechanical threshold in diabetic hyperalgesic rats were obviously decreased, and a small number of A(delta) units (4/24) and C units (2/18) produced increased spontaneous activities. Intraperitoneal injection of indomethacin in diabetic hyperalgesic rats significantly relieved mechanical hyperalgesia, and resulted in a decrease in spontaneous afferent activities of the A(delta) units and C units. Subcutaneous injection of exogenous PGE(2) into the diabetic hyperalgesic and control rats produced a significant decrease in mechanical threshold of the A(delta) units and C units, and elicited discharge from 3 A(delta) units (3/24) and 1 C unit (1/18) in diabetic hyperalgesic rats and from 2 A(delta) units (2/13) in control rats. The present data suggest that the synthesis and release of PGs are increased in diabetic neuropathy, PGs can sensitize and /or activate A(delta) units and C units and elicit hyperalgesia and allodynia in diabetic rats.
