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Why we don’t get confused.

Neurons receiving a signal from the taste buds in your mouth, find their receptors by specific molecular “portrait”.


Gustatory papilla of tongue. (Photo: MBBS Study Stuff / Flickr.com.)

Gustatory papilla with different receptors and conducting neurons that serve as an intermediary, transmitting the taste signal to the brain neurons. Neurons are the mediators work each with its own type of receptor. (Illustration: Lee et al. / Nature 2017.)”

The question in the title may seem strange: we don’t confuse sweet with bitter, because bitter sweet and we have different taste buds. In General, as you know, the basic five tastes – sweet, sour, bitter, salty and umami, or the taste of protein; to each of them has its own type of receptor cells that sit on the surface of the tongue, and he felt a acid, salt, etc., give the appropriate signal to the brain.

Sour receptor will never respond to salty, bitter – sweet, because we do not get confused . (It is worth Recalling that there is one main taste – the taste of water, and are responsible for it sour receptors, but essentially it does not change.)

However, the fact that the taste receptor cells live very long, only two weeks. To replace the lost receptors stem cells in the epithelium of the tongue give rise to a replacement, and here the problem occurs – new cells needs to establish proper contact with the conducting neurons. That is, the cell feeling a sweet taste, should be connected to the neural line, which transmit a signal sweet – but not bitter, not sour, not salty and not protein. How is it that when a permanent replacement receptors do not occur any confusion?

Not so long ago we wrote about semaphorin proteins – they help the processes of nerve cells to grow in the right direction when there is the formation of the motor neural circuits. In the case of taste buds is also not without semaphorins.

Researchers from the Medical Institute of Howard Hughes analyzed the molecular portrait of bitter and sweet receptors, and found that bitter synthesize a lot of semaphorin 3A, and sweet – semaphorin 7. When the bitter receptors would shut off the synthesis of semaphorin 3A, the neurons that were supposed to take readings with bitter receptor cells began to stretch and other receptors for sweet, salty and protein. In an article in Nature the authors write that nearly half of “bitter” host neurons formed a contact with a receptor. And the same thing happened when sweet receptors would shut off their semaphorin 7.

If the proteins semaphorin swaps, that is sweet receptors activated by bitter semaphorin 3A, it necessarily affected the structure of neural circuits, and behavior of laboratory mice: sweet buds formed connections with bitter conducting neurons, and mouse started to mix the different tastes. (Probably their semaphorin have other receptors, just researchers them while not tested, limiting the two.)

In other words, the sense of taste is protected from confusion due to the molecular portrait of receptor cells, which, despite the fact that are updated very often still support the correct neural contacts with a set of special proteins.

While experimenting on mice, the results likely can be extended to human organs of taste and the neural “wires” that serve them, held in rodents in a similar way. However, there remain some ambiguities on how it work semaphorin, it is believed that they serve not so much bait for growing neurons, how many bogey – that is, the neural semaphorin not allow the process to come closer to the cage, which synthesizes the protein.

To find out all the details on how the molecular work permits and limitations on cell growth during the formation of the gustatory neural pathways will need further investigation.

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