For years now, we’ve believed that the protein responsible for our brain’s ability to detect bitter, sweet and savory foods depends solely on G protein-coupled receptor signaling with the transient receptor potential melastatin 5 (TRPM5) protein, crowning it as the sole gatekeeper for these flavors and our ability to distinguish and recognize them, often activated by high levels of intracellular calcium. That’s why smoking seems to result in a taste loss for many people– nicotine inhibits the TRPM5 channel, effectively dismantling its role.
However, a new study from the University at Buffalo suggests that TRPM5 may not be the sole protein involved in this processing of taste. Another protein, TRPM4, seems to also be involved in performing a similar role. In the university’s experiments, mice with the TRPM4 drank sugar-water enthusiastically, and also reacted strongly against quinine, a very bitter crystalline compound. In contrast, the mice without the protein had difficulty distinguishing and detecting the savory, sweet and bitter flavors. The research indicates that there is some superfluity in the taste transduction pathways, and is critically important for human survival– many poisons and harmful substances often have a particular taste, and if undetectable due to a defect in either one of these proteins, can cause serious injuries or risks. The research overall, seems to support that both protein TRPM4 and TRPM5 are key players in terms of taste transduction, and the loss of either one of them can cause a severe decrease in taste sensitivity.
Not much beyond the basics is known about TRPM4, but we do know that like TRPM5, TRPM4 is an ion channel protein, and is located on the taste cells. Both of the channels open when a certain food of either savory, sweet or bitter taste land on the taste cells on the tongue, and the cells automatically start firing electrical impulses at the nerve endings. These electrical impulses will then travel all the way to the brain, arriving at the gustatory complex within the sensory lobe on the cerebral cortex.
Exploring the taste transduction pathways further more, opens more doors to new treatments to existing problems regarding eating habits and patterns. After all, taste plays a big role in regulating appetite. Malnutrition, either by excessive or minimal eating, can be caused if these proteins don’t operate properly, so closer studies on these proteins would be nearly revolutionary. The study, led by PhD candidates Kathryn Medler and Debarghya Dutta Banik, is set to be published in the Proceedings of the National Academy of Sciences (PNAS).
In an older 2013 study, Medler’s team had found that the taste cells of overweight mice were less sensitive to sweets than the cells of slimmer counterparts. Medler states that a possibility is that trouble detecting the flavor can lead obese mic to eat more in order to receive the same amount of payoff. There’s not a doubt that this scenario could perhaps apply to humans as well, so furthering research in taste signaling and transduction will not only allow for new discoveries, but also contributes to human health and potential treatments.
(Now published on the Huffington Post!)
Neurologic 