The Release of Spinal Prostaglandin E2 and the Effect of Nitric Oxide Synthetase Inhibition During Strychnine-Induced Allodynia
- 1 September 2001
- journal article
- research article
- Published by Wolters Kluwer Health in Anesthesia & Analgesia
- Vol. 93 (3) , 728-733
- https://doi.org/10.1097/00000539-200109000-00037
Abstract
The removal of spinal glycinergic inhibition by intrathecal strychnine produces an allodynia-like state in rodents. Our objective was to measure spinal prostaglandin E2 (PGE2) release during strychnine-allodynia and examine the effects of Nω-nitro-l-arginine (l-NOARG), an inhibitor of nitric oxide synthetase. Under halothane, rats were fitted with intrathecal and spinal microdialysis catheters, and microelectrodes implanted into the locus coeruleus for measurement of catechol oxidation current (CAOC) using voltammetry. Animals were then administered urethane and treated as follows: 1) baseline control 10 min, intrathecal strychnine (40 μg) 10 min, 10 min of hair deflection, and 2) 10-min control followed by intrathecal strychnine (40 μg) with hair deflection for 60 min. Spinal dialysate samples were collected for PGE2 levels determined by using immunoassay. In separate experiments, the effect of intrathecal strychnine (40 μg) followed by hair deflection was studied in rats pretreated with intrathecal l-NOARG (50 nmol). After intrathecal strychnine, hair deflection significantly increased spinal PGE2 release (619% ± 143%), locus coeruleus CAOC (181% ± 6%), and mean arterial pressure (123% ± 2%) PKeywords
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