May 14, 1999

A research team at the MGH and Harvard University has identified a molecule that may be key to the process by which the chemical signals called pheromones are turned into nerve impulses travelling to the brain in rodents. The discovery, which appears in the May 11 issue of Proceedings of the National Academy of Science, has two unusual aspects: the molecule is most similar to one that insects use to receive visual signals, and it is produced by a gene that is defective in humans.

"This finding doesn’t mean that we all should throw out our expensive perfumes and colognes," says first author Emily Liman, PhD. "Instead it suggests that humans probably process pheromones through a different mechanism than most other mammals do." The research team also includes David Corey, PhD, of the MGH, and Catharine Dulac, PhD, of Harvard. All team members also are researchers with the Howard Hughes Medical Institute.

Many aspects of animal behavior — particularly those relating to courtship and mating — are known to be controlled by pheromones. Although they are detected by the nose, most pheromones are received by a different structure than that used for receiving odors. While pheromones are believed to play a role in the timing of women’s menstrual cycles, any larger role in human physiology is poorly understood.

The molecule identified by the MGH/Harvard team, called TRP2, is an ion channel, which plays a key role in transforming chemical signals into nerve impulses. Found only in the structure where pheromones are detected, TRP2 is similar to a molecule fruit flies use to detect light. In humans, the TRP2 gene does not produce a functioning protein, supporting evidence that humans process pheromones through different structures than do rodents.