Wednesday, February 11, 2015

Food for Thought

Courtesy of E. Robertson, who looked it up

The Sense of Taste

Taste is the ability to respond to dissolved molecules and ions called tastants.
Humans detect taste with taste receptor cells. These are clustered in taste buds and scattered in other areas of the body. Each taste bud has a pore that opens out to the surface of the tongue enabling molecules and ions taken into the mouth to reach the receptor cells inside.
There are five primary taste sensations:

Properties of the taste system.

  • A single taste bud contains 50–100 taste cells representing all 5 taste sensations (so the classic textbook pictures showing separate taste areas on the tongue are wrong).
  • Each taste cell has receptors on its apical surface. These are transmembrane proteins which
    • admit the ions that give rise to the sensation of salty;
    • bind to the molecules that give rise to the sensations of sweet, bitter, and umami.
  • A single taste cell seems to be restricted to expressing only a single type of receptor (except for bitter receptors).
  • A stimulated taste receptor cell triggers action potentials in a nearby sensory neuron leading back to the brain.
  • However, a single sensory neuron can be connected to several taste cells in each of several different taste buds.
  • The sensation of taste — like all sensations — resides in the brain [evidence].
  • And in mice, at least, the sensory neurons for four of the tastes (not sour) transmit their information to four discrete areas of the brain.

Salty

In mice, perhaps humans, the receptor for table salt (NaCl) is an ion channel that allows sodium ions (Na+) to enter directly into the cell depolarizing it and triggering action potentials in a nearby sensory neuron.
In lab animals, and perhaps in humans, the hormone aldosterone increases the number of these salt receptors. This makes good biological sense:
  • The main function of aldosterone is to maintain normal sodium levels in the body.
  • An increased sensitivity to sodium in its food would help an animal suffering from sodium deficiency (often a problem for ungulates, like cattle and deer).

Sour

Sour receptors detect the protons (H+) liberated by sour substances (acids). This closes transmembrane K+ channels which leads to depolarization of the cell [Link], and the release of the neurotransmitter serotonin into its synapse with a sensory neuron.

Sweet

Sweet substances (like table sugar — sucrose) bind to G-protein-coupled receptors (GPCRs) at the cell surface.
  • Each receptor contains 2 subunits designated T1R2 and T1R3 and is
  • coupled to G proteins.
  • The complex of G proteins has been named gustducin because of its similarity in structure and action to the transducin that plays such an essential role in rod vision.
  • Activation of gustducin triggers a cascade of intracellular reactions:
    • production of the second messengers inositol trisphosphate (IP3) and diacylglycerol (DAG) which
    • releases intracellular stores of Ca++ which
    • allows in the influx of Na+ ions depolarizing the cell and causing the
    • release of ATP, which
    • triggers action potentials in a nearby sensory neuron.
The hormone leptin inhibits sweet cells by opening their K+ channels. This hyperpolarizes the cell making the generation of action potentials more difficult. Could leptin, which is secreted by fat cells, be a signal to cut down on sweets?

Bitter

The binding of substances with a bitter taste, e.g., quinine, phenylthiocarbamide [PTC], also takes place on G-protein-coupled receptors that are coupled to gustducin and the signaling cascade is the same as for sweet (and umami).
Humans have genes encoding 25 different bitter receptors ("T2Rs"), and each taste cell responsive to bitter expresses a number (4–11) of these genes. (This is in sharp contrast to the system in olfaction where a single odor-detecting cell expresses only a single type of odor receptor.)
Despite this — and still unexplained — a single taste cell seems to respond to certain bitter-tasting molecules in preference to others.
The sensation of taste — like all sensations — resides in the brain. Transgenic mice that
  • express T2Rs in cells that normally express T1Rs (sweet) respond to bitter substances as though they were sweet;
  • express a receptor for a tasteless substance in cells that normally express T2Rs (bitter) are repelled by the tasteless compound.
So it is the activation of hard-wired neurons that determines the sensation of taste, not the molecules nor the receptors themselves.

Umami

Umami is the response to salts of glutamic acid — like monosodium glutamate (MSG) a flavor enhancer used in many processed foods and in many Asian dishes. Processed meats and cheeses (proteins) also contain glutamate.
The binding of amino acids, including glutamic acid, takes place on G-protein-coupled receptors that are coupled to heterodimers of the protein subunits T1R1 and T1R3. The signaling cascade that follows is the same as it is for sweet and bitter.

Taste Receptors in Other Locations

Taste receptors have been found in several other places in the body. Examples:
  • Bitter receptors (T2Rs) are found on the cilia and smooth muscle cells of the trachea and bronchi [View] where they probably serve to expel inhaled irritants;
  • Sweet receptors (T1Rs) are found in cells of the duodenum. When sugars reach the duodenum, the cells respond by releasing incretins. These cause the beta cells of the pancreas to increase the release of insulin.
So the function of "taste" receptors appears to be the detection of chemicals in the environment — a broader function than simply taste.

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