Many reports have indicated that electro-acupuncture analgesia (EAA) was mediated by endorphins. Among them is B-endorphin which can be released from the anterior lobe of the pituitary. To examine the role of B-endorphin in EAA and observe CNS metabolic (functional) and behavioral effects of dexamethasone the present study employed the (14C) 2-deoxyglycose (2DG) method. Seventeen adult male Sprague-Dawley rats in five groups received the following different types of somesthetic stimulation to examine the local cerebral glucose utilization (LCGU) and tail-flick response latency: control group (N = 3), pain group (N = 4), EA group (N = 3), pain + EA group (N = 3; from another ongoing study) and dexamethasone group (N = 4). Dexamethasone reduced tail-flick response latency in response to electroacupuncture, and produced metabolic (functional) changes in a number of CNS structures implicated in electroacupuncture produced analgesia effects (some changes were statistically significant, many others were not). Specific brain structures exhibiting statistically significant changes (p less than 0.05) in LCGU when compared to the pain + EA group are: the parafascicular and habennlar nuclei of the thalamus and the posterior cingulate gyrus. In comparison of dexamethasone group with the other four experimental groups of rats, the following trend in LCGU changes was observed: pain + EA group greater than pain group = EA group = dexamethasone group greater than control group. In addition, dexamethasone had a sedative effect. The results suggest that dexamethasone is reducing EAA and having suppressive effects on CNS metabolism and behavior.