According to researchers in Maryland, a single gene is the reason why some people perceive pain more acutely than others, reports CBS News Correspondent Christopher Glenn.
Dr. George R. Uhl of Johns Hopkins University, lead researcher of a study in the Proceedings of the National Academy of Sciences, says the discovery of pain sensitivity has far-reaching implications.
"We hope to be able to take this information and use it to develop a genetic test that can predict individuals' differences in pain susceptibility and especially differences in morphine responsiveness to pain," he told CBS News.
In the study, Uhl and his colleagues show that differences in pain perception are due to a variation on the surface of nerve cells of a molecule called the mu opiate receptor.
Studies of humans and mice show that the number of these receptors directly affects sensitivity to pain, and that the receptors, in turn, are linked to a single gene called the mu opiate receptor gene.
The mu receptor works by bonding with natural chemicals, called peptides, that help to diminish the sensation of pain, Uhl said.
When there are lots of these receptors, the perception of pain is diminished, researchers say. But when the receptors are reduced in number or missing altogether, the nerve cell takes up fewer peptides and even a small stimulus is perceived as painful.
The number of these receptors is controlled by the action of the mu opiate receptor gene, Uhl said.
To measure the gene's effect, Uhl used eight different strains of mice with different levels of expression, or activity, of the mu receptor gene. Mice with a vigorous gene had many receptors, while those with a weak gene had few.
The different mouse strains' reaction to pain was tested and Uhl said the number of mu receptors was directly linked to the animals' reaction to pain, specifically, how long it took them to react to nonharmful levels of temperature and pressure.
Mice with no mu receptors reacted to temperatures or pressures that were only two-thirds of what it took to cause a pain reaction in mice with the normal number of receptors. For mice with 50 percent fewer receptors, the pain reaction came at about 80 percent of normal, researchers say.
Uhl said studies of human volunteers have shown that the number of mu receptors varies from patient to patient, and that pain perception is directly linked to the number of mu receptors.
He said researchers now are attempting to connect these differences directly to the number of mu receptors and to pain perception.
Uhl said the mu opiate receptor is the primary target of morphine and some other opiate drugs that are key to controlling serious pain, such as in cancer.
By understanding how the mu receptor gene causes differences in pain perception, doctors one day hope to match prescription drugs to an individual patient's pain threshold.