Who felt it not, smelt it not

People with a genetic inability to feel pain also can’t detect odors

People who feel no pain due to a particular rare genetic defect also can’t smell anything, a new study finds. The unexpected discovery shows that nerves that detect pain and odors rely on the same protein to transmit information to the brain.

Researchers examined three people who have mutations in the SCN9A gene and can’t feel pain. All of the people had broken multiple bones without feeling any pain, and two had given birth painlessly. But none were aware that they also couldn’t smell a thing.

None of the study participants could distinguish balsamic vinegar, orange, mint, coffee or perfume from plain water, even when researchers poured on so much perfume and vinegar that the scents were unbearable to people with a normal sense of smell, an international team of researchers reports online March 23 in Nature.

It may not be so strange that none of the people realized that they lacked a sense of smell. “If this was a genetic defect from birth they wouldn’t even know what they were missing,” says Graeme Lowe, a neurophysiologist at the Monell Chemical Senses Center in Philadelphia who was not involved in the study.

As oblivious as the patients were to their smell deficit, the scientists had been equally clueless that smell and pain shared a common communication gateway.

Researchers had previously shown that SCN9A controls pain sensitivity in people (SN Online: 3/8/10). The gene makes a protein, called a sodium channel, that lets sodium pass in through a nerve cell’s membrane when the nerve detects something painful. That flood of sodium sends an electrical signal racing down a long tendril, called an axon, toward the brain.

In the new study, the team discovered that odor-detecting nerve cells have the same sodium channel at the tips of their axons. In those cells, the channel controls the release of a chemical called glutamate, which in turn sparks electrical communication with odor-processing centers in the brain.

Because the sodium channel is missing in people with SCN9A mutations, the messages sent by pain- and odor-sensing nerves never actually make it to the brain.

“It was completely surprising that these two sensory systems would use the same sodium channel,” says Frank Zufall, a neurophysiologist at the University of Saarland School of Medicine in Homburg, Germany. “But it’s clearly not needed for all senses.” None of the people with the faulty gene had hearing or vision problems. The researchers plan to test whether those people have a sense of taste, and whether taste cells also use the sodium channel to communicate.

Although the people weren’t bothered by not being able to smell, mice engineered to lack the sodium channel in smell-sensing nerve cells had a tough time. Baby mice are blind and rely on their sense of smell to guide them to their mother’s milk. Without the sodium channel, baby mice were underweight and mother mice couldn’t locate babies that had gotten out of the nest. Adult mice lacking the protein also wandered into territory marked with the scent of foxes — a place normal mice strictly avoided. “These [mutant] mice have no chance in nature,” Zufall says.

Some pharmaceutical companies are already working on painkilling drugs that would block the sodium channel’s activity. But the new study suggests that such drugs could have the side effect of eliminating smell, Lowe says. Because odor is an important component in creating the flavor of a food, people’s ability to taste would also be compromised, he says.

Tina Hesman Saey is the senior staff writer and reports on molecular biology. She has a Ph.D. in molecular genetics from Washington University in St. Louis and a master’s degree in science journalism from Boston University.

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