Biologists have discovered a protein that may be responsible for the phantom sensation of bitterness

Biologists have discovered a protein that interrupts molecular signals of bitterness. If taste cells do not have this protein, animals and humans cannot get rid of the unpleasant aftertaste. Scientists are sure that the absence of the anti-bitter molecule may be the cause of the phantom sensation of bitterness.

Taste buds are not only needed to enjoy food. The sense of taste is one of the ways to obtain information about the quality, safety and nutritional value of food. The lungs and intestines also sense taste. But they do not need such sensations for cognition, but to stimulate appetite and ease breathing.

Humans and other mammals recognize sweet, piquant (spicy, hot), bitter, salty and sour tastes. "When you drink tonic, quinine molecules "switch on" taste cells, which begin sending a signal to the brain that the tonic is bitter," write scientists from US research centers, explaining that the mechanism for informing the brain about bitterness and other taste sensations is well studied, there are no blank spots in it. But it is not entirely clear how the activated informant cells "switch off" after the bitter food has ceased to irritate them.

Biologists explain that activation of taste cells is associated with an increase in the concentration of calcium ions (Ca ²⁺ ) in the cytosol, the liquid part of the cell's contents. In order for the brain to stop "feeling" taste, calcium ions must leave the cytosol of taste cells.

Molecular biologist Liquan Huang of the Monell Chemical Senses Center and his colleagues decided to understand the mechanisms by which taste cells clear calcium ions. The biologists discovered that the receptors that recognize bitterness have too much of the protein Serca3.

"This molecule is a member of the family of inner membrane Ca ²⁺ -ATPases (SERCAs). It 'confiscates' calcium by forcing it into the network of intracellular membranes called the endoplasmic reticulum," the biologists write in a paper published today in PLoS ONE. To test whether Serca3 really does stop bitter signals, the scientists created mice that lacked the gene for this protein (Serca3-KO mice).

During the experiment, mice tried solutions of food chemicals from five taste groups. To do this, the researchers allowed the mice to drink distilled water and a solution of one of the taste chemicals (sugar, salt, quinine, etc.) for forty-eight hours. After two days, the animals were given a break for several days, after which drinking bowls with distilled water and another solution of the taste chemical appeared in the cage again. During the experiment, the scientists measured the amount of liquid drunk and monitored the animals' behavior.

It turned out that mice without the Serca3 protein experience a stronger and longer aversion to bitter water than normal animals. They snorted and spat more and stayed away from the water bowl for longer. “This is because they feel the bitter aftertaste for too long,” the scientists explain the results of their observations.

Biologists note that aversion to bitter water is noticeable not only in behavior. In experimental mice, the glossopharyngeal nerve reacted to bitter water more strongly than in animals from the control group. Biologists did not find any reliable significant differences in relation to salty and sour taste chemicals. But they noted that the sensitivity to sweet and spicy tastes changes in Serca3-KO mice. As it turned out later, these changes are associated with the compensatory appearance of a related compound - the Serca2 protein. By the way, in people with a heightened perception of bitterness, the taste for sweet and spicy also changes.

"Our results explain why people perceive taste differently," the authors of the study conclude. "Although this is fundamental work, it also has practical significance. For example, it is possible to develop drugs for people who experience phantom tastes."

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