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Rockefeller researchers provide the first functional evidence for mammalian pheromone receptors

mutant mice, and it is consistent with reports from other researchers who have removed the VNO from male mammals.

When the nerve cells in the VNO of the mutant mice were exposed to mouse pheromones, the team discovered that certain pheromones no longer elicited a physiological response in these cells. Other pheromones, however, still stimulate these nerve cells, indicating that the sensory deficit is specific. The authors coined a new term for this selective chemosensory deficit: a specific avnosmia, analogous to specific anosmias to certain 'common' odorants reported in many cases over the past decades, both in mouse and human. "The specific avnosmia may perturb the normal detection of pheromones and cause the behavioral abnormalities we observed," speculates Del Punta.

Whether a functional VNO is present in humans is controversial. The role of pheromones in human behavior also has not been clearly defined. The Mombaerts team had shown earlier that the human genome harbors 5 putative pheromone receptor genes that could be functional. The genome of the mouse, by contrast, has at least 140 receptor genes of this type, and the mutant strain of mice described in the Nature paper misses precisely 16 of these.

"Our work has shown for the first time that these are pheromone receptors in mice. This in turn will stimulate research in functional characterization of the counterparts of these genes in human," concludes Mombaerts.


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Contact: Joseph Bonner
bonnerj@mail.rockefeller.edu
212-327-8998
Rockefeller University
4-Sep-2002


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