ABSTRACT
For the past 50 years it has been known that sensitivity to pain and responses to analgesics are variable among people (1-3). This variability is due to a combination of genetic and environmental factors. These influences underlie the considerable clinical differences observed in painrelated syndromes. The finding of several endogenous receptor ligands is likely to be why the study of genetics of pain has been overlooked. This pharmacological approach has led to the discovery of detailed processes in pain transmission and modulation (4,5).
