Glucocorticoid-mediated enhancement of glutamatergic transmission may outweigh anti-inflammatory effects under conditions of neuropathic pain.

ABSTRACT: At the clinical level comorbidity between chronic pain and dysfunctional hypothalamus-pituitary-adrenal (HPA) axis is well established. We aimed to identify causal relationships in a model of neuropathic pain (chronic constriction injury, CCI) by studying the effects of glucocorticoid receptor agonist (dexamethasone) and antagonist (RU-486) administration on pain behavior and spinal biochemical mediators. Daily injections were performed in Sprague Dawley rats. Weight, plasma corticosterone levels and mechanical pain thresholds were assessed before and during 21 days post-CCI. At days four and 21 we investigated the mRNA expression of spinal mediators. In the dexamethasone-injected group, we observed a diminution of body weight and plasma corticosterone levels during the 21 days post surger

SUBMITTER: Le Coz GM 

PROVIDER: S-EPMC3950185 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature