Ben-Shahar stresses the differences between chemosensation in the nose and in the lung. The cells in the nose are neurons, he points out, each with a narrowly tuned receptor, and their signals must be woven together in the brain to interpret our odor environment.
The cells in the airways are secretory not neuronal cells and they may carry more than one receptor, so they are broadly tuned. Instead of sending nerve impulses to the brain, they flood local nerves and muscles with serotonin and neuropeptides. "They are possibly designed," he said, "to elicit a rapid, physiological response if you inhale something that is bad for you."
The different mechanisms explain why cognition plays a much stronger role in taste and smell than in coughing in response to an irritant. It is possible, for example, to develop a taste for beer. But nobody learns not to cough; the response is rapid and largely automatic.
The scientists suspect these pulmonary neuroscretory cells contribute to the hypersensitivity of patients with Chronic Obstructive Pulmonary Disease (COPD) to airborne irritants. COPD is a group of diseases including emphysema that are characterized by coughing, wheezing, shortness of breath and chest tightness.
When the scientists looked at the airway tissues from patients with COPD they discovered that they had more of these neurosecretory cells than airway tissues from healthy donors.
Of mice and men
As a geneticist Ben-Shahar would like to go farther, knocking out genes to make sure that the derangement of neurosecretory cells isn't just correlated with airway diseases but instead suffices to produce it.
But there is a problem. "For example, a liver from a mouse and a liver from a human are pretty similar, they express the same types of cells. But the lungs from different mammalian species are often ve
|Contact: Diana Lutz|
Washington University in St. Louis