The functioning of the cells that allow us to perceive the taste of foods is discovered.
IN 1994, RICHARD AXEL AND LINDA BUCK at the College of Physicians and Surgeons of Columbia University in New York announced the discovery of proteins in the membrane of nasal cells that capture odorant molecules and make olfaction possible. The news caused a great stir, but it failed to satisfy researchers interested in the related problem of taste. Two years later another team of biochemists at Columbia, Gwendolyn Wong, Kimberley Gannon, and Robert Margolskee, published the results of a study of gustducin, a protein found in the papillary cells of the tongue that had been cloned in 1992 but whose function was unknown. They observed that inhibiting the synthesis of gustducin in the taste cells of mice caused these animals to lose their aversion to bitter flavors and, still more surprisingly, their sensitivity to sweet molecules.
Taste begins when a sapid molecule binds with receptors or ion channels in the membrane of a papillary sensory cell. Once the electrical potential of the papillary cell is sufficiently modified as the result of a series of reactions, the cell commences to excite neurons, which, little by little, convey information to the brain.
Not all taste molecules act in the same fashion. Whereas hydrogen ions (sour taste) and sodium ions (salt taste) act directly on the channels of taste cell membranes, immediately modifying the electrical potential of the cell by adding their electrical charge to its total charge, compounds of sweet, bitter, and other tastes (licorice, for example) bind to molecules known as receptors—no doubt proteins—that are located in the cell membrane, in contact with the extracellular environment.
It is thought that these receptors are paired with other previously identified proteins, the G-proteins, which trigger the emission of molecules known as second messengers that act within the cell. Nonetheless, the receptors are evanescent because they form only a weak bond with taste molecules. This is inconvenient from the scientific point of view, but, gastronomically speaking, it is an advantage: If taste molecules formed too strong a bond with receptors, we would not perceive the rapid succession of tastes in a dish.
Before the discovery of these receptors, Margolskee and his colleagues had begun investigating G-proteins, which are particularly abundant in the taste cells of the tongue. Using a method of genetic amplification involving the polymerase enzyme, they multiplied the number of genes of the alpha-subunits of several G-proteins, notably gustducin, which is uniquely expressed in such papillary cells.
These studies confirmed similarities between taste and vision. Gustducin was found to resemble a class of G-proteins found in the receptor cells of the eye known as transducins. Moreover, the Columbia team detected the transducin that is specific to the cones and rods of the eye in taste receptor cells.
The Eye and the Papilla
The resemblance proved to be enlightening. For if papillary cells function like the cells in the eye, then gustducin and transducin activate an enzyme that diminishes cyclic adenosine monophosphate production. In this hypothesis, the shortage of this second messenger would either modify the ion channels of the cell membrane and associated enzymes or disrupt the exchange of calcium ions between the inside and outside of the cell.
To test this hypothesis, the Columbia team inactivated the gene that codes for the alpha-subunit of gustducin and studied the behavior of mice born with this inhibited gene when they were offered various sapid solutions to drink. At the same time the neurobiologists recorded the electrical signals from the chorda tympani, a branch of the facial nerve that conveys gustatory information to the brain. The reactions were normal for salt and sour flavors but much weaker for bitter compounds such as quinine sulfate and denatonium benzo ate and for sucrose (ordinary cane sugar) and a normally very intense synthetic sweetener.
Why was the perception of bitter and sweet not completely nullified? The neurophysiologists reasoned that because transducin plays a role, along with gustducin, in the perception of these tastes, the fact that it was not eliminated meant that they continued to be perceived, albeit to a lesser degree. Therefore their next experiment will investigate the consequences of inhibiting the genes for both transducin and gustducin.