I Can’t Sleep - Taste Buds | Relaxing Bedtime Reading for Sleep

Episode Date: December 5, 2019

Relax with calm bedtime reading about taste buds to ease insomnia and restless nights. This gentle episode explores how these tiny sensory organs on the tongue help us detect sweet, salty, sour, bitter, and umami flavors. Benjamin’s soothing cadence turns biology into a peaceful learning experience, helping your mind unwind while discovering how taste connects to smell, health, and daily life. There’s no whispering or hypnosis—just calm, fact-filled storytelling to reduce stress, quiet racing thoughts, and invite restful sleep. Press play and drift off peacefully. Want More? Request a Topic: https://www.icantsleeppodcast.com/request-a-topic Ad-Free Episodes: https://icantsleep.supportingcast.fm/ Shop Sleep-Friendly Products: https://www.icantsleeppodcast.com/sponsors Join the Discussion on Discord: https://discord.gg/myhGhVUhn7 This content is derived from the Wikipedia article on Taste Bud, available under the Creative Commons Attribution-ShareAlike (CC BY-SA) license. Read the full article: Wikipedia – Taste Bud. Happy sleeping! Learn more about your ad choices. Visit megaphone.fm/adchoices

You're listening to a Glassbox media podcast. What if I told you that most of the modern day self-help advice you've been hearing could actually make you worse? The key to a better life isn't about feel-good gimmicks that sound catchy. The Mentally Stronger Podcast gives you access to a licensed therapist who shares science-backed tools that will actually change your life. Hi, I'm Amy Morin, psychotherapist, mental strength trainer, and international best-selling author. In each episode, we cover research-back strategies, like how to stop relying on willpower and start creating habits for lasting change. And the five mental strength-building exercises you can do from your couch. I also speak to world-class experts like Dr. Nicole Kane, who shares how to permanently heal anxiety by addressing the root cause.

With over 200 episodes in our catalog, this podcast is for you if you're ready to crush self-doubt, conquer challenges, become stronger than ever with therapist-approved strategies that can change your life. Listen to Mentally Stronger with Therapist Amy Morin, wherever you get your podcasts. Welcome to the I Can't Sleep Podcast, where I read random articles from across the web to bore you to sleep with my soothing voice. I'm your host, Benjamin Boster. Today's episode is a request from one of our listeners, Zeke Bot. He requested an episode about taste buds. So today's episode is from a Wikipedia article titled Taste Bud, and I'm also adding on something new, mostly because this episode is a little bit shorter than normal. We're going to

add a related article called taste receptor. Taste buds contain the taste receptor cells, which are also known as gustatory cells. The taste receptors are located around the small structures known as papillet found on the upper surface of the tongue, soft palate, upper esophagus, a cheek, and epiglottis. These structures are involved in detecting the five elements of taste perception, salty, sour, bitter, sweet, and umami. A popular myth assigns these different tastes to different regions of the tongue. In reality, these tastes can be detected by any area of the tongue. Via small openings, in the tongue epithelium called taste pores, parts of the food dissolved in saliva come into contact with the taste receptors. These are located on top of the taste receptor cells that

constitute the taste buds. The taste receptor cells send information detected by clusters of various receptors and ion channels to the custatory areas of the brain via the 7th, 9th, and 10th cranial nerves. On average, the human tongue has 2,000 to 8,000 taste buds. The average lifespan of these are estimated to be 10 days. The taste buds on the tongue sit on raised protrusions of the tongue surface called papillae. There are four types of lingual papillus, all except one containing taste buds. Fungi form papillet, as the name suggests, these are slightly mushroom-shaped. if looked at in longitudinal section. These are present mostly at the dorsal surface of the tongue as well as at the sides.

Inervated by facial nerve, foliate papillet. These are ridges and grooves towards the posterior part of the tongue found at the lateral borders. Inervated by facial nerve, anterior papillet, and glossophorangeal nerve, posterior papillus. circumvalet papillet. There are only about 10 to 14 of these papillus on most people, and they are present at the back of the oral part of the tongue. They are arranged in a circular-shaped row just in front of the sulcus terminus of the tongue. They are associated with ducks of funebner's glands and are innervated by the glossophorangial nerve. Philiform papillet The most numerous type, but do not contain taste buds. They are characterized by increased keratinization and are involved in the mechanical aspect of providing abrasion. The bud is formed by two kinds of cells, supporting cells and gustatory cells.

The supporting, sustentacular cells, are mostly arranged like the staves of a cask, and form an outer envelope for the bud. Some, however, are found in the interior of the bud between the gustatory cells. The gustatory taste cells, which are chemoreceptors, occupy the central portion of the bud. They are spindle-shaped and each possesses a large spherical nucleus near the middle of the cell. The peripheral end of the cell terminates at the gustatory pore in a fine hair filament. a gustatory hair.

The central process passes toward the deep extremity of the bud, and there ends in single or bifurcated varicosities. The nerve fibrials, after losing their medullary sheaths, enter the taste bud, and in fine extremities between the gustatory cells. Other nerve fibrials ramify between the supporting cells and terminate in the fine extremities. These, however, are believed to be nerves of

ordinary sensation and not gustatory. Salt, sweet, sour, and umami tastes causes depolarization of the taste cells, although different mechanisms are applied. Bitter causes an internal release of CA2-plus. No external CA2 plus is required. A taste receptor is a type of receptor which facilitates the sensation of taste. These receptors are of four types. When food or other substances enter the mouth,

molecules interact with saliva and are bound to taste receptors in the oral cavity and other locations. Molecules which give a sensation of taste are considered sapid. Taste receptors are divided into two families. Type 1, sweet, first characterized in 2001. Type 2, bitter, first characterized in 2000. 2000. In humans, there are 25 known different bitter receptors. In cats, there are 12. In chickens, there are three, and at mice, there are 35 known different bitter receptors. Visual,

alfactive, sepictive, the perception of tastes. Tragiminal, hot, cool, mechanical, all contribute to the perception of taste. Of these transient, receptor potential Cachian channel subfamily 5, number 1, T-R-P-V-1, vaniloid receptors are responsible for the perception of heat from some molecules, such as Capsatchin, and a CMR-1 receptor is responsible for the perception of cold for molecules, such as menthol, eucalyptus, and isulin. The gustatory system consists of taste receptor cells in taste buds. Taste buds, in turn, are contained in structures called papillae.

There are three types of papillae involved in taste. Fungiform papillet, foliate papillet, and circumvalet papillet. The fourth time philiform papillet did not contain taste buds. Beyond the papillet, taste receptors are also in the palate and early parts of the digestive system like the larynx and upper esophagus. There are three cranial nerves that innervate the tongue, the vagus nerve, glossophorangeal nerve, and the facial nerve. The glossophorangeal nerve and the cortotempany branch of the facial nerve innervate the TAS1R and TAS2R taste receptors. Next to the taste receptors in on the tongue, the gut epithelium is also equipped with a subtle chemosensory system. system that communicates the sensory information to several effector systems involved in the regulation of appetite, immune responses, and gastrointestinal motility.

In 2010, researchers found bitter receptors in lung tissue, which cause airways to relax when a bitter substance is encountered. They believe this mechanism is evolutionarily adaptive because it helps clear lung infections, but could also be exploited to treat asthma and chronic obstructive pulmonary disease. Taste helps to identify toxins, maintain nutrition, and regulate appetite, immune responses, and gastrointestinal motility. Five basic tastes are recognized today. salty, sweet, bitter, sour, and umami. Salty and sour taste sensations are both detected through ion channels. Sweet, bitter, and umami tastes, however, are detected by way of G-protein-coupled taste receptors.

In addition, some agents can function as taste modifiers as miraclein or circlin for sweet or staribin to mask bitter. The standard bitter, sweet, or umami taste receptor is a G-protein-coupled receptor with seven transmembrane domains. Ligin binding at the taste receptors activate second messenger cascades to depolarize the taste cell. Gustusin is the most common taste G.A. Sabinit having a major role in TAS2R bitter taste reception. Gustafin is a homologue for transducin, a G-protein involved in vision transduction. Additionally, taste receptors share the use of the TRPM-5 ion channel. The TAS 1R1 plus TAS1R3 heterotomer receptor functions as an umami receptor, responding to L-amino-acid binding, especially L-glutamate. The umami taste is most frequently associated with the food additive monosodium glutamate, MSG,

and can be enhanced through the binding of inocene monophosphate IMP and guanazine monophosphate GMP molecules. TAS1R1 plus 3 expressing cells are found mostly in the fungi form papillet at the tip and edges of the tongue, and palate taste receptor cells in the roof of the mouth. These cells are shown to synapse upon the cordotempany nerves to send their signals to the brain, although some activation of the glossophorangeal nerve has been found. Alternative candidate Umami taste receptors include splice variants of metabotropic glutamate receptors,

M-G-L-U-R-4, and M-G-L-U-R-1, and the N-Menthal-D-Aspartate-Ty glutamate-ion channel receptor. The T-A-S-1-R-2 plus T-A-S-1-R-3 heterotamer receptor functions as the sweet receptor by binding to a wide variety of sugars and sugar substitutes. T-A-S-1-2-plus-3 expressing cells are found in CERodemes, circumvalet papillae and foliot papillae near the back of the tongue and palate taste receptor cells in the roof of the mouth. These cells are shown to synapse upon the cordotimony and glossophorangeal nerves to send their signals to the brain.

The TAS 1R3 homotermar also functions as a sweet receptor in much the same way as TAS 1R2 plus 3. but has decreased sensitivity to sweet substances. Natural sugars are more easily detected by the TAS-1R-3 receptor than sugar substitutes. This may help explain why sugar and artificial sweeteners have different tastes. Genetic polymorphisms in TAS 1R3 partly explain the difference in sweet taste perception and sugar consumption between people of African-American ancestry and people of European and Asian ancestries. The TAS 2R proteins function as bitter taste receptors.

There are 43 human TAS2R genes, each of which, excluding the five pseudogenes, lacks introns and codes for a GPCR protein. These proteins, as opposed to TAS-1-R proteins, have short extracellular domains, and are located in circumvalet, papillate, papillet, pallet, foliotpapal, and epiglottous taste buds, with reduced expression in fungi form papillae. Though it is certain that multiple TAS-2Rs are expressed in one taste receptor cell, it is still debated whether mammals can distinguish. distinguish between the tastes of different bitter ligands. Some overlap must occur, however, as there are far more bitter compounds than there are TAS-2-R genes.

Common bitter ligands include cyclohexamide, denotonium, prop 6N Prop-Pil2 Thyaracil, PTC, phenylthiocarbamide, and B-Gluco-Pyranisone. Signal transduction of bitter stimuli is accomplished via the A subunit of Gustusin. This G-protein subunit activates a taste phosphodiasterase and decrease cyclic nucleotide levels. Further steps in the transduction pathway are still unknown. The BY subunit of Gustin also mediates taste by activating IP3, a Nossal triphosphate and D-A-G diglyceride. These second messengers may open gated ion channels or may cause release of internal calcium.

Though all TAS 2Rs are located in gustusin-containing cells, knockout of Gostasin does not completely abolish sensitivity to bitter compounds, suggesting a redundant mechanism for bitter tasting. unsurprising, given that a bitter taste generally signals the presence of a toxin. One proposed mechanism for gestussin-independent bitter tasting is via ion-channel interaction by specific bitter ligands, similar to the ion-channel interaction which occurs in the tasting of sour and salty stimuli. One of the best research TAS-2R proteins is TAS-2R-38, which contributes to the tasting of both PROP and PTC. It is a first taste receptor whose polymorphisms are shown to be responsible for differences in

taste perception. Current studies are focused on determining other such taste phenotype determining of polymorphisms. More recent studies show that genetic polymorphisms in other bitter taste receptor genes influence bitter taste perception of caffeine, quinine, and denatonium benzoid. Historically, it was thought that the sour taste was produced solely when free hydrogen ions directly depolarized taste receptors.

However, specific receptors for sour taste with other methods of action are now being proposed. HCN1 and HCN4 HCN channels were two such proposals. Both of these receptors are cyclic nucleotide gated channels. The two ion channels suggested to contribute to sour taste are ACCN1 and TASK1. Various receptors have also been proposed for salty tastes, along with the possible taste detection of lipids, complex carbohydrates, and water. evidence for these receptors is however shaky at best and is often unconvincing in mammal studies. For example, the proposed ENAC receptor for sodium detection can only be shown to contribute to sodium taste in drosophilia.

An enzyme connected to the sour receptor transmits information about carbonated water, A possible taste receptor for fat, CD36, has been identified. CD36 has been localized to the circumvalet and foliate papillus, which are present in taste buds and where lingual lipase is produced, and research has shown that the CD36 receptor binds long-chain fatty acids. Differences in the amount of CD-36 expression in human subjects was associated with their ability to taste fats, creating a case for the receptor's relationship to fat tasting.

Further research into the CD-36 receptor could be useful in determining the existence of a true fat-tasting receptor. GPR 120 and GPR-40 have been implicated to respond to oral fat, and their absence leads to reduced fat preference and reduced net. neural response to orally administered fatty acids. TRPM has been shown to be involved in oral fat response and identified as a possible oral fat receptor, but recent evidence presents it as primarily a downstream actor. Human bitter taste receptor genes are named TAS2R1 and TAS2R64, with many gaps due to non-existent

genes, pseudogenes, or proposed genes that have not been annotated to the most recent human genome assembly. Many bitter taste receptor genes also have confusing synonym names with several different gene names referring to the same gene. In many species, taste receptors have shown loss of function. The evolutionary process of which taste receptors lost their function is believed to be an adaptive evolution, where it is associated with feeding ecology to drive specialization and bifurcation of taste receptors. Out of all the taste receptors, bitter, sweet, and umami are shown to have a correlation between inactivation of taste receptors and feeding behavior. However, there are no strong evidences that support any vertebrates are missing the bitter taste receptor genes. The sweet taste receptor is one of the

taste receptors where the function has been lost. In mammals, the predominant sweet taste receptor is the type 1 taste receptor, TAS 1R2, TAS1R3. Some mammalian species such as cats and vampire bats have shown inability to taste sweet. In these species, the cause of loss of function of the sweet receptor is due to the pseudogenization of TAS1R2. The pseudogenization of TAS 1R2 is also observed in non-mammalian species such as chickens and tongueless western clawed frog, and these species also show the inability to taste sweet. The pseudogenization of TAS 1R2 is widespread and independent in the order carnivora. Many studies have shown that the pseudogenization of taste receptors is caused by a deleterious mutation in the

the open reading frames, ORF. In a study, it was found that in non-feline carnivores species, these species showed ORF disrupting mutations of TAS 1R2, and they occurred independently among the species. They also show high variants in their lineages. It is hypothesized that the pseudogenization of TAS 1R2 occurred through Convergent Evolution, where, Carnivorous species lost their ability to taste sweet because of dietary behavior.

Umami is also a taste receptor where the function has been lost in many species. The predominant umami taste receptors are TAS 1R1, TAS 1R3. In two lineages of aquatic mammals, including dolphins and sea lions, TAS 1R1 has been found to be sedative. The pseudogenization of TAS-1R-1 has also been found in terrestrial carnivorous species. While the panda belongs to the order carnivora, it is herbivorous where 99% of its diet is bamboo, and it cannot taste umami. Genome sequence of the panda shows that its TAS-1R-1 gene is pseudogenized.

It was found that in all species in the order carnivora, except the panda, the open reading frame was maintained. In Panda, the non-sanonymous to synonymous substitutions ratio was found to be much higher than other species in order carnivora. This data correlates with fossil records date of the panda to show where panda switched from carnivore to herbivore diet. Therefore, the loss of function of Umami and Panda is hypothesized to be caused by dietary change

where the panda became less dependent on meat. However, these studies do not explain herbivores such as horses and cows that have maintained the TAS-1R-1 receptor. Overall, the loss of function of the taste receptor is an evolutionary process that occurred due to a dietary change in species.