Chapter 6. Hearing, Balance, Taste, and Smell
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by Tanya Lewis, LiveScience In waters from Florida to the Caribbean, dolphins are showing up stranded or entangled in fishing gear with an unusual problem: They can't hear. More than half of stranded bottlenose dolphins are deaf, one study suggests. The causes of hearing loss in dolphins aren't always clear, but aging, shipping noise and side effects from antibiotics could play roles. "We're at a stage right now where we're determining the extent of hearing loss [in dolphins], and figuring out all the potential causes," said Judy St. Leger, director of pathology and research at SeaWorld in San Diego. "The better we understand that, the better we have a sense of what we should be doing [about it]." Whether the hearing loss is causing the dolphin strandings -- for instance, by steering the marine mammals in the wrong direction or preventing them from finding food -- is also still an open question. Dolphins are a highly social species. They use echolocation to orient themselves by bouncing high-pitched sound waves off of objects in their environment. They also "speak" to one another in a language of clicks and buzzing sounds. Because hearing is so fundamental to dolphins' survival, losing it can be detrimental. A 2010 study found that more than half of stranded bottlenose dolphins and more than a third of stranded rough-toothed dolphins had severe hearing loss. The animals' hearing impairment may have been a critical factor in their strandings, and all rescued cetaceans should be tested, the researchers said in the study, detailed in the journal PLOS ONE. © 2013 Discovery Communications, LLC.
Researchers have found in mice that supporting cells in the inner ear, once thought to serve only a structural role, can actively help repair damaged sensory hair cells, the functional cells that turn vibrations into the electrical signals that the brain recognizes as sound. The study in the July 25, 2013 online edition of the Journal of Clinical Investigation reveals the rescuing act that supporting cells and a chemical they produce called heat shock protein 70 (HSP70) appear to play in protecting damaged hair cells from death. Finding a way to jumpstart this process in supporting cells offers a potential pathway to prevent hearing loss caused by certain drugs, and possibly by exposure to excess noise. The study was led by scientists at the National Institutes of Health. Over half a million Americans experience hearing loss every year from ototoxic drugs — drugs that can damage hair cells in the inner ear. These include some antibiotics and the chemotherapy drug cisplatin. In addition, about 15 percent of Americans between the ages of 20 and 69 have noise-induced hearing loss, which also results from damage to the sensory hair cells. Once destroyed or damaged by noise or drugs, sensory hair cells in the inner ears of humans don’t grow back or self-repair, unlike the sensory hair cells of other animals such as birds and amphibians. This has made exploring potential pathways to protect or regrow hair cells in humans a major focus of hearing research.
By Emma Tracey BBC News, Ouch An online magazine for the deaf community, Limping Chicken, recently ran an item on how deaf and hearing people sneeze differently. The article by partially deaf journalist Charlie Swinbourne got readers talking - and the cogs started turning at Ouch too. Swinbourne observes that deaf people don't make the "achoo!" sound when they sneeze, while hearing people seem to do it all the time - in fact, he put it in his humorous list, The Top 10 Annoying Habits of Hearing People. Nor is "achoo" universal - it's what English-speaking sneezers say. The French sneeze "atchoum". In Japan, it's "hakashun" and in the Philippines, they say "ha-ching". Inserting words into sneezes - and our responses such as "bless you" - are cultural habits we pick up along the way. So it's not surprising that British deaf people, particularly users of sign language, don't think to add the English word "achoo" to this most natural of actions. For deaf people, "a sneeze is what it should be... something that just happens", says Swinbourne in his article. He even attempts to describe what an achoo-free deaf sneeze sounds like: "[There is] a heavy breath as the deep pre-sneeze breath is taken, then a sharper, faster sound of air being released." Very little deaf-sneeze research exists, but a study has been done on deaf people and their laughter. BBC © 2013
Link ID: 18355 - Posted: 07.08.2013
by Helen Fields When a bat moves in for the kill, some moths jiggle their genitals. Researchers made the observation by studying three species of hawk moths—big moths that can hover—in Malaysia. They snared the insects with bright lights, tied tiny leashes around their waists, and let them fly while bat attack sounds played. All three species responded to the noises with ultrasound—which they made by shaking their private parts, the team reports online today in Biology Letters. Males have a structure they use for hanging onto females when they mate; to make the sound, they scrape a patch of large scales on the structure against the very end of their abdomen , letting out two bursts of rapid clicks. Females also make a sound, but the researchers aren't sure how. The scientists don't know exactly what the sounds are for, either. The noise may warn the bats that they're trying to mess with a fast-moving, hard-to-catch piece of prey, or it might jam the bat's ultrasound signals. Either way, the racy display may save their lives. © 2010 American Association for the Advancement of Science
By Scicurious Sometimes, funny stories really bring out the wonder of the human body. You can get orgasms triggered in your feet, because of overlap in the sensory cortex. Receptors that are involved in narcolepsy are also involved in how much you eat. And knocking out receptors that regulate taste…can make you sterile? Who knew? Let’s start with taste. We taste because the chemicals in foods hit receptors on our tongues. Receptors for sweet, salt, bitter, sour, and umami (which can commonly be thought of as “savory”). Now, a receptor isn’t just a single protein, it’s actually several protein subunits working together to function. So, for example, the receptor subunit TAS1R3 is a subunit that can play two different tasting roles. When combined with one other subunit, it helps to sense sweet (like saccharin), and when combined with another, if helps you taste umami (like MSG, which is definitely umami flavored). If you get rid of the gene for TAS1R3, you end up with an animal that can’t detect either sweet or umami very well. There’s another subunit that is covered in this paper as well, GNAT3. GNAT3, instead of being specific for something like sweet or bitter, instead plays a role in “basic taste“. But these two protein subunits are not JUST expressed on the tongue and in the gastrointestinal tract. They are expressed elsewhere in the body…and especially in the testicles. © 2013 Scientific American
David Derbyshire Every year Robert Hodgson selects the finest wines from his small California winery and puts them into competitions around the state. And in most years, the results are surprisingly inconsistent: some whites rated as gold medallists in one contest do badly in another. Reds adored by some panels are dismissed by others. Over the decades Hodgson, a softly spoken retired oceanographer, became curious. Judging wines is by its nature subjective, but the awards appeared to be handed out at random. So drawing on his background in statistics, Hodgson approached the organisers of the California State Fair wine competition, the oldest contest of its kind in North America, and proposed an experiment for their annual June tasting sessions. Each panel of four judges would be presented with their usual "flight" of samples to sniff, sip and slurp. But some wines would be presented to the panel three times, poured from the same bottle each time. The results would be compiled and analysed to see whether wine testing really is scientific. The first experiment took place in 2005. The last was in Sacramento earlier this month. Hodgson's findings have stunned the wine industry. Over the years he has shown again and again that even trained, professional palates are terrible at judging wine. "The results are disturbing," says Hodgson from the Fieldbrook Winery in Humboldt County, described by its owner as a rural paradise. "Only about 10% of judges are consistent and those judges who were consistent one year were ordinary the next year. © 2013 Guardian News and Media Limited
By Helen Briggs BBC News Our perception of how food tastes is influenced by cutlery, research suggests. Size, weight, shape and colour all have an effect on flavour, says a University of Oxford team. Cheese tastes saltier when eaten from a knife rather than a fork; while white spoons make yoghurt taste better, experiments show. The study in the journal Flavour suggests the brain makes judgements on food even before it goes in the mouth. More than 100 students took part in three experiments looking at the influence of weight, colour and shape of cutlery on taste. The researchers found that when the weight of the cutlery confirms to expectations, this had an impact on how the food tastes. For example, food tasted sweeter on the small spoons that are traditionally used to serve desserts. Colour contrast was also an important factor - white yoghurt eaten from a white spoon was rated sweeter than white yoghurt tasted on a black spoon. Similarly, when testers were offered cheese on a knife, spoon, fork or toothpick, they found that the cheese from a knife tasted saltiest. "How we experience food is a multisensory experience involving taste, feel of the food in our mouths, aroma, and the feasting of our eyes," said Prof Charles Spence and Dr Vanessa Harrar. BBC © 2013
Keyword: Chemical Senses (Smell & Taste)
Link ID: 18315 - Posted: 06.26.2013
Melissa Dahl TODAY The video will melt your heart: A deaf little boy is stunned when he hears his father’s voice for the first time after receiving an auditory brainstem implant. “Daddy loves you,” Len Clamp tells his 3-year-old son, Grayson, in a video that was recorded May 21 but is going viral today. (He signs the words, too, to be sure the boy would understand.) Grayson was born without cochlear nerves, the “bridge” that carries auditory information from the inner ear to the brain. He’s now the among the first children in the U.S. to receive an auditory brainstem implant in a surgery done at the University of North Carolina in Chapel Hill, N.C., led by UNC head and neck surgeon Dr. Craig Buchman. The device is already being used in adults, but is now being tested in children at UNC as part of an FDA-approved trial. It’s similar to a cochlear implant, but instead of sending electrical stimulation to the cochlea, the electrodes are placed on the brainstem itself. Brain surgery is required to implant the device. "Our hope is, because we're putting it into a young child, that their brain is plastic enough that they'll be able to take the information and run with it," Buchman told NBCNews.com.
By NICHOLAS BAKALAR Obesity in adolescents is associated with a range of cardiovascular and other health risks. Now a new study adds one more: hearing loss. Several studies have demonstrated the association of obesity with hearing loss in adults, but now researchers examining records of a nationwide sample of 1,488 boys and girls ages 12 to 19 have found the same association in teenagers. The study appeared online in The Laryngoscope. The researchers controlled for various factors, including poverty, sex, race and previous exposure to loud noises. They found that being at or above the 95th percentile for body mass index — the definition of obesity in teenagers — was independently associated with poorer hearing over all frequencies, and with almost double the risk of low-frequency hearing loss in one ear. They suggest that this may represent an early stage of injury that will later progress to both ears, as it does in adults. The reason for the connection is not known, but the scientists suggest that inflammation induced by obesity may be a factor in organ damage. “It’s quite possible that early intervention could arrest the progression,” said the lead author, Dr. Anil K. Lalwani, a professor of otolaryngology at Columbia University. “This is another reason to lose weight — but not to lose hope.” Copyright 2013 The New York Times Company
By NICHOLAS BAKALAR Hearing loss in older adults increases the risk for hospitalization and poor health, a new study has found, even taking into account other risk factors. Researchers analyzed data on 529 men and women over 70 with normal hearing, comparing them with 1,140 whose hearing was impaired, most with mild or moderate hearing loss. The data were gathered in a large national health survey in 2005-6 and again in 2009-10. The results appeared in The Journal of the American Medical Association. After adjusting for race, sex, education, hypertension, diabetes, stroke, cardiovascular disease and other risks, the researchers found that people with poor hearing were 32 percent more likely to be hospitalized, 36 percent more likely to report poor physical health and 57 percent more likely to report poor emotional or mental health. The authors acknowledge that this is an association only, and that there may be unknown factors that could have affected the result. “There has been a belief that hearing loss is an inconsequential part of aging,” said the lead author, Dr. Frank R. Lin, an associate professor of otolaryngology at Johns Hopkins. “But it’s probably not. Everyone knows someone with hearing loss, and as we think about health costs, we have to take its effects into account.” Copyright 2013 The New York Times Company
Link ID: 18267 - Posted: 06.13.2013
A team of NIH-supported researchers is the first to show, in mice, an unexpected two-step process that happens during the growth and regeneration of inner ear tip links. Tip links are extracellular tethers that link stereocilia, the tiny sensory projections on inner ear hair cells that convert sound into electrical signals, and play a key role in hearing. The discovery offers a possible mechanism for potential interventions that could preserve hearing in people whose hearing loss is caused by genetic disorders related to tip link dysfunction. The work was supported by the National Institute on Deafness and Other Communication Disorders (NIDCD), a component of the National Institutes of Health. Stereocilia are bundles of bristly projections that extend from the tops of sensory cells, called hair cells, in the inner ear. Each stereocilia bundle is arranged in three neat rows that rise from lowest to highest like stair steps. Tip links are tiny thread-like strands that link the tip of a shorter stereocilium to the side of the taller one behind it. When sound vibrations enter the inner ear, the stereocilia, connected by the tip links, all lean to the same side and open special channels, called mechanotransduction channels. These pore-like openings allow potassium and calcium ions to enter the hair cell and kick off an electrical signal that eventually travels to the brain where it is interpreted as sound. The findings build on a number of recent discoveries in laboratories at NIDCD and elsewhere that have carefully plotted the structure and function of tip links and the proteins that comprise them. Earlier studies had shown that tip links are made up of two proteins — cadherin-23 (CDH23) and protocadherin-15 (PCDH15) — that join to make the link, with PCDH15 at the bottom of the tip link at the site of the mechanotransduction channel, and CDH23 on the upper end. Scientists assumed that the assembly was static and stable once the two proteins bonded.
Link ID: 18265 - Posted: 06.13.2013
By ROBERT J. ZATORRE and VALORIE N. SALIMPOOR MUSIC is not tangible. You can’t eat it, drink it or mate with it. It doesn’t protect against the rain, wind or cold. It doesn’t vanquish predators or mend broken bones. And yet humans have always prized music — or well beyond prized, loved it. In the modern age we spend great sums of money to attend concerts, download music files, play instruments and listen to our favorite artists whether we’re in a subway or salon. But even in Paleolithic times, people invested significant time and effort to create music, as the discovery of flutes carved from animal bones would suggest. So why does this thingless “thing” — at its core, a mere sequence of sounds — hold such potentially enormous intrinsic value? The quick and easy explanation is that music brings a unique pleasure to humans. Of course, that still leaves the question of why. But for that, neuroscience is starting to provide some answers. More than a decade ago, our research team used brain imaging to show that music that people described as highly emotional engaged the reward system deep in their brains — activating subcortical nuclei known to be important in reward, motivation and emotion. Subsequently we found that listening to what might be called “peak emotional moments” in music — that moment when you feel a “chill” of pleasure to a musical passage — causes the release of the neurotransmitter dopamine, an essential signaling molecule in the brain. When pleasurable music is heard, dopamine is released in the striatum — an ancient part of the brain found in other vertebrates as well — which is known to respond to naturally rewarding stimuli like food and sex and which is artificially targeted by drugs like cocaine and amphetamine. © 2013 The New York Times Company
Link ID: 18251 - Posted: 06.10.2013
by Kim Krieger The song of the cicada has been romanticized in mariachi music, used to signify summer in Japanese cinematography, and cursed by many an American suburbanite wishing for peace and quiet. Despite the bugs' ubiquity, scientists haven't uncovered how they sing so loudly—some are as noisy as a jet engine—and why they don't expend much energy doing it. But researchers reported in Montreal yesterday at the 21st International Congress on Acoustics that they now have the answer. The detailed mechanism of the cicada's song is far from fully understood, says Paulo Fonseca, an animal acoustician at the University of Lisbon who was not involved in the project. The work by the researchers "is innovative and paves our way to a better understanding of this complex system allowing such small animals to produce such powerful sound." Cicadas aren't just a natural curiosity. Small devices that produce extremely loud noises while requiring very little power appeal to the U.S. Navy, which uses sonar for underwater exploration and communication. Derke Hughes, a research engineer at the Naval Undersea Warfare Center in Newport, Rhode Island, says that the loudest cicadas can make a noise 20 to 40 dB louder than the compact off-the-shelf RadioShack speaker in his office using the same amount of power. Intrigued, he and his colleagues used microcomputed tomography)—a kind of CT scan that picks up details as small as a micron in size—to image a cicada's tymbal, which helps the insect make its deafening chirp. © 2010 American Association for the Advancement of Science
By Susan Milius Cockroaches that don’t fall for traps’ sweet poisons have evolved taste cells that register sugar as bitter. In certain groups of the widespread German cockroach (Blattella germanica), nerve cells that normally detect bitter, potentially toxic compounds now also respond to glucose, says entomologist Coby Schal of North Carolina State University in Raleigh. The “bitter” reaction suppresses the “sweet” response from other nerve cells, and the roach stops eating, Schal and his colleagues report in the May 24 Science. Normally roaches love sugar. But with these populations, a dab of jelly with glucose in it makes them “jump back,” Schal says. “The response is: ‘Yuck! Terrible!’” This quirk of roach taste explains why glucose-baited poison traps stopped working among certain roaches, Schal says. Such bait traps combining a pesticide with something delicious became popular during the mid-1980s. But in 1993, Jules Silverman, also a coauthor on the new paper, reported roaches avoiding these once-appealing baits. “This is a fascinating piece of work because it shows how quickly, and how simply, the sense of taste can evolve,” says neurobiologist Richard Benton of the University of Lausanne in Switzerland. What pest-control manufacturers put in their roach baits now, and whether some still use glucose, isn’t public, Schal says. But humankind’s arms race with cockroaches could have started long ago, “in the caves,” he says. In this back-and-forth struggle, it’s important “to understand what the cockroach is doing from a molecular basis.” © Society for Science & the Public 2000 - 2013
By JANE E. BRODY Sugar, and especially the high-fructose corn syrup that sweetens many processed foods and nearly all soft drinks, has been justly demonized for adding nutritionally empty calories to our diet and causing metabolic disruptions linked to a variety of diseases. But a closer look at what and how Americans eat suggests that simply focusing on sugar will do little to quell the rising epidemic of obesity. This is a multifaceted problem with deep historical roots, and we are doing too little about many of its causes. More than a third of American adults and nearly one child in five are now obese, according to the Centers for Disease Control and Prevention. Our failure to curtail this epidemic is certain to exact unprecedented tolls on health and increase the cost of medical care. Effective measures to achieve a turnaround require a clearer understanding of the forces that created the problem and continue to perpetuate it. The increase in obesity began nearly half a century ago with a rise in calories consumed daily and a decline in meals prepared and eaten at home. According to the Department of Agriculture, in 1970 the food supply provided 2,086 calories per person per day, on average. By 2010, this amount had risen to 2,534 calories, an increase of more than 20 percent. Consuming an extra 448 calories each day could add nearly 50 pounds to the average adult in a year. Sugar, it turns out, is a minor player in the rise. More than half of the added calories — 242 a day — have come from fats and oils, and another 167 calories from flour and cereal. Sugar accounts for only 35 of the added daily calories. Copyright 2013 The New York Times Company
By Laura Beil When chemists Richard Marshall and Earl Kooi started fiddling with cornstarch, the powder made from the dense insides of corn kernels, their intention was to turn glucose, which is easily produced from the starch, into fructose, which is sweeter. The idea wasn’t that far-fetched. The two sugar molecules are cousins, both made from the same atomic parts slightly rearranged. The duo’s experiment, which took place at the Corn Projects Refining Company in Argo, Ill., was a success. Marshall and Kooi discovered that the bacterium Aeromonas hydrophila produced an enzyme that could reconfigure the components of glucose from corn like so many Lego blocks. It was the first leap forward for a food industry dream: a mass-produced glucose-fructose-blend sweetener that would free commercial food manufacturers from the historical volatility of cane sugar crops. The scientists announced their triumph in a short report in Science in 1957. There the discovery sat in quiet obscurity for almost two decades, until a worldwide spike in sugar prices sent manufacturers scrambling. By the end of the 1980s, high fructose corn syrup had replaced cane sugar in soft drinks, and it soon became popular among makers of baked goods, dairy products, sauces and other foods. Few consumers seemed to care until 2004, when Barry Popkin, a nutrition scientist at the University of North Carolina at Chapel Hill, along with George Bray, at the Pennington Biomedical Research Center in Baton Rouge, La., published a commentary in the American Journal of Clinical Nutrition pointing out that the country’s obesity crisis appeared to rise in tandem with the embrace of high fructose corn syrup by food producers. That shift began in the early 1970s — just about the time Japanese researchers, who had noted Marshall and Kooi’s experiment with keen interest, overcame the technical hurdles of industrial production. © Society for Science & the Public 2000 - 2013
by Meera Senthilingam Malaria parasites give mosquitoes a keener sense of smell, it seems. A small-scale study in the lab finds that mosquitoes infected by the parasite are three times as likely as uninfected mosquitoes to respond to human odours. If the same results are seen in malaria-carrying mosquitoes in the wild, it could lead to new ways to combat the disease. Female anopheles mosquitoes are attracted to the chemicals in human odours, which help them find the source of blood they need to grow their eggs. When these mosquitoes carry Plasmodium falciparum – the most lethal form of malaria parasite – the likelihood that they will target humans rises. "We knew already that mosquitoes bite more often when they're infected. They probe the skin more frequently," says James Logan from the London School of Hygiene and Tropical Medicine. To quantify the effect – and try to work out its cause – Logan and his colleagues infected some lab-grown Anopheles gambiae mosquitoes with Plasmodium parasites, while leaving others uninfected. They then tested how both groups were attracted to human smells. Mosquitoes are particularly attracted to foot odours, so Logan's team used nylon stockings containing the volatile chemicals produced by our feet. Over a period of three minutes, Plasmodium-infected mosquitoes landed and attempted to bite the stockings around 15 times on average. By contrast, the uninfected mosquitoes attempted to bite only around five times on average during that time. © Copyright Reed Business Information Ltd.
Keyword: Chemical Senses (Smell & Taste)
Link ID: 18160 - Posted: 05.16.2013
Zoe Cormier A study of two ancient hominins from South Africa suggests that changes in the shape and size of the middle ear occurred early in our evolution. Such alterations could have profoundly changed what our ancestors could hear — and perhaps how they could communicate. Palaeoanthropologist Rolf Quam of Binghamton University in New York state and his colleagues recovered and analysed a complete set of the three tiny middle-ear bones, or ossicles, from a 1.8-million-year-old specimen of Paranthropus robustus and an incomplete set of ossicles from Australopithecus africanus, which lived from about 3.3 million to around 2.1 million years ago. The ossicles are the smallest bones in the human body, and are rarely preserved intact in hominin fossils, Quam says. In both specimens, the team found that the malleus (the first in the chain of the three middle-ear bones) was human-like — smaller in proportion compared to the ones in our ape relatives. Its size would also imply a smaller eardrum. The similarity between the two species points to a “deep and ancient origin” of this feature, Quam says. “This could be like bipedalism: a defining characteristic of hominins.” It is hard to draw conclusions about hearing just from the shape of the middle-ear bones because the process involves so many different ear structures, as well as the brain itself. However, some studies have shown that the relative sizes of the middle-ear bones do affect what primates can hear2. Genomic comparisons with gorillas have indicated that changes in the genes that code for these structures might also demarcate humans from apes3. © 2013 Nature Publishing Group
by Michael Balter Researchers debate when language first evolved, but one thing is sure: Language requires us not only to talk but also to listen. A team of scientists now reports recovering the earliest known complete set of the three tiny middle ear bones—the malleus ("hammer"), incus ("anvil"), and stapes ("stirrup")—in a 2.0-million-year-old skull of Paranthropus robustus, a distant human relative found in South Africa (see photo). Reporting online today in the Proceedings of the National Academy of Sciences, the researchers found that the malleus of P. robustus, as well one found earlier in the early human relative Australopithecus africanus, is similar to that of modern humans, whereas the two other ear bones most closely resemble existing African and Asian great apes. The team is not entirely sure what this precocious appearance of a human-like malleus means. But since the malleus is attached directly to the eardrum, the researchers suggest that it might be an early sign of the high human sensitivity to middle-range acoustic frequencies between 2 and 4 kilohertz—frequencies critical to spoken language, but which apes and other primates are much less sensitive to. © 2010 American Association for the Advancement of Science
Ed Yong Many moths have evolved sensitive hearing that can pick up the ultrasonic probes of bats that want to eat them. But one species comes pre-adapted for anything that bats might bring to this evolutionary arms race. Even though its ears are extremely simple — a pair of eardrums on its flanks that each vibrate four receptor cells — it can sense frequencies up to 300 kilohertz, well beyond the range of any other animal and higher than any bat can squeak. “A lot of previous work has suggested that some bats have evolved calls that are out of the hearing range of the moths they are hunting. But this moth can hear the calls of any bat,” says James Windmill, an acoustical engineer at the University of Strathclyde, UK, who discovered the ability in the greater wax moth (Galleria mellonella). His study is published in Biology Letters1. Windmill's collaborator Hannah Moir, a bioacoustician now at the University of Leeds, UK, played sounds of varying frequencies to immobilized wax moths. As the insects “listened”, Moir used a laser to measure the vibrations of their eardrums, and electrodes to record the activity of their auditory nerves. The moths were most sensitive to frequencies of around 80 kilohertz, the average frequency of their courtship calls. But when exposed to 300 kilohertz, the highest level that the team tested, the insects' eardrums still vibrated and their neurons still fired. © 2013 Nature Publishing Group