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I was always under the impression that the auditory hairs located deep within the ear, past the ear drum, are microscopic.
After taking a shower today, I was softly padding my outer ear with some tissue paper to dry any moisture, when some wax just got attached to it. What was unusual was that there were some hairs on it (3-5 perhaps, overlapping) that were about half a centimeter in length.
Are these just regular hairs that grow in the inner/outer ear? Or are they the ones that actually aid in hearing (the ones I thought were microscopic).
My question is to verify whether or not these hair shafts I observed are used in auditory perception. Either way, are these supposed to fall off?
Those are just ordinary hairs growing in your ear, like the kind you find in your nose and, if you are fortunate, on the top of your head. The "hair cells" of the inner ear aren't really "hairs" at all, they are totally different, and you would never find them falling out of your ear.
Hairs like on your head are protein filaments produced by follicles in the skin.
Hair cells in the inner ear, on the other hand, are sensory epithelial cells with stereocilia, which are protrusions of the cell membrane. Those membrane protrusions have mechanically gated channels which are coupled to nearby protrusions; when the whole cell is pushed one way or the other, that influences the mechanical stress on those channels and they open and close, which produces an electrical signal that can be sensed by the auditory nerve.
These special 'hair cells' are way way deep in your ear, past your ear drum, past three little bones that conduct sound into your cochlea. If you are touching those, you are in bad shape indeed - this is very very unlikely under normal circumstances.
Of the five senses, sight and hearing are often felt to be the most important. They allow us to interact with each other and our environment, and the loss of either sense can be devastating. Worldwide, an estimated 39 million people have severe vision loss and 360 million people have disabling hearing loss (1,2). Scientists have spent many decades studying the causes of vision and hearing loss, as well as working to understand how images and sounds are transmitted to and represented in the brain. After years of research, they are now creating technologies that can at least partially restore these senses. These technologies are called neuroprosthetics and take the form of devices that connect to brain cells to deliver information that the brain can no longer receive on its own, often due to injury or disease.
How do neuroprosthetics work?
The brain is comprised of specialized cells called neurons. One of the things that makes these cells unique is that they send information via electrical signals, which travel quickly through large networks of neurons to coordinate various brain functions. Scientists have taken advantage of this electrical signaling in designing neuroprosthetic devices (3). Electrodes can be used to deliver electrical current to neurons, and neurons will respond to that current similarly to how they respond to a signal from another cell. Therefore, scientists can create devices to replace damaged cells as long as they know how to replicate the electrical signals normally sent by those cells.
Scientists have been able to create neuroprosthetics for hearing and sight based on research investigating how auditory and visual neurons work. In the case of hearing, sound waves vibrate the eardrum, which transmits the vibrations to a chain of small bones inside the ear. Ultimately, those mechanical vibrations are turned into electrical signals by inner ear sensory cells called hair cells. Hair cells then deliver these signals to the auditory nerve, which transmits the message from the inner ear to the brain (4). The process is similar for vision, although in this case, sensory cells called photoreceptors located at the back of the eye in a tissue called the retina produce electrical signals when stimulated by light. They communicate with the optic nerve, which travels from the eye into the brain to pass on visual information (5). Scientists are studying how different sounds and images stimulate specific groups of hair cells and photoreceptors to produce particular patterns of electrical signals. Armed with this information, they have started making neuroprosthetic devices to help people whose hair cells or photoreceptors have been damaged.
A neuroprosthetic for hearing
The oldest form of neuroprosthetic is the cochlear implant, which was approved for use by the U.S. Food and Drug Administration (FDA) in the mid-1980’s (6). This device can be beneficial for people who are deaf, severely hard-of-hearing, or who have experienced profound hearing loss due to disease or injury, enabling them to once again hear sounds in their environment and carry on conversations. The implant is only recommended for people whose ears are so damaged that they are not helped by hearing aids, which work by making sounds louder. The reason the cochlear implant can help people with severe hearing impairment is that it bypasses the damaged area of the ear and directly stimulates the auditory nerve itself (7), which must be present and functional for the device to work (8).
Figure 1. This illustration depicts the components of a cochlear implant (7). The external machinery is located near the ear and sends electrical signals through the skin. These signals must travel to the electrode array positioned deep within the spiral-shaped cochlea.
The cochlear implant consists of an external component, containing a microphone, a speech processor, and a transmitter, and an internal component, comprised of a receiver/stimulator that sits just beneath the skin and sends signals to an electrode array positioned deep in the inner ear (Figure 1). Sound in the environment is picked up by the microphone, analyzed and converted to electrical signals by the processor, and sent through the skin by the transmitter. The receiver picks up these signals and sends them to the electrode array, which is positioned carefully so that it can deliver patterns of electrical activity to the auditory nerve, similar to those delivered by healthy hair cells (8). The implant allows people to regain some hearing however, it does not restore completely normal hearing and requires that recipients spend time learning to interpret what they hear with the device. To date, over 200,000 people worldwide have received implants (7). Scientists continue to work on the technology of the external machinery and the design and positioning of the internal electrode to improve performance and provide more naturalistic sound (9).
A neuroprosthetic for vision
The newest advance in neuroprosthetics is a prosthetic for vision, the first artificial retina, approved by the FDA in February of this year (10). This device, called the Argus II, is the result of the U.S. Department of Energy’s (DOE’s) Artificial Retina Project. Six DOE national laboratories, four universities, and private industry worked together to develop the technology (11). The artificial retina works similarly to the cochlear implant, except this device uses a small camera attached to a pair of glasses to pick up images, and the device’s processor converts these images into light and dark pixels. The device’s receiver then turns this information into electrical signals and sends them to a sheet of photoreceptor-stimulating electrodes sitting on the retina. The photoreceptors finally send the information to the optic nerve and the brain (5, Figure 2).
Figure 2. The external hardware of the artificial retina looks like a pair of sunglasses with a miniature camera attached (top left). The receiver is on the eye and the processor is worn on a belt and not shown in this illustration. Signals are sent from the receiver to the implanted sheet of electrodes, which sits on the retina at the back of the eye and stimulates remaining photoreceptors (top right and bottom) (5).
At this time, the only people who are approved for this device are those who have lost their vision due to retinitis pigmentosa, a disorder in which the photoreceptors deteriorate (10). While their vision has largely been lost, they may still have some functional photoreceptors, which are necessary to receive the signal from the electrodes (5). Because this device only transmits information on light and dark regions, people do not get back normal vision, but are able to see things based on contrast, such as borders and outlines of objects or lights against a dark background. Due to the limited nature of what patients can see, this device has only been given to those with severe blindness. Even though it seems limited, people who have used the Argus II say they would rather see something than nothing and feel that the device helps them navigate the world more easily (10). Scientists are currently working on improving this technology and obtaining approval to use this system to treat people who have lost vision as a result of other causes.
The future of neuroprosthetics
The cochlear implant and artificial retina are only two of the many neuroprosthetics under development. Scientists are also beginning to work on technology that goes in the reverse direction, allowing electrical signals from the brains of disabled individuals to control external devices that can help them regain mobility and communication. Among these technologies are robotic arms controlled by electrodes implanted in the brains of paralyzed patients and robotic exoskeletons controlled by brain activity designed to help stroke survivors regain motion (3, 12). With the rapid progress in this field, scientists hope that it will soon be feasible for neuroprosthetics to improve the lives of people suffering from a variety of nervous system-related disorders.
What is the mechanotransduction channel in hearing that has evaded scientists for decades?
1 having cloned and sequenced the acetylcholine receptor in 1983. The sodium channel identification made a big splash in the field Numa's publication has been cited in 895 publications.
So as a postdoc in the 1980s, Gillespie probably wasn't alone in his enthusiasm about the channel. He was young, curious, and had the notion that he would be able to identify, at a molecular level, exactly what comprised the channel. The hair cell mechanotransduction channel had just been proposed.
Since that 1983 paper by Corey & Hudspeth (cited 250 times), reams of data have supported the channel's existence. But the narrative of the hair cell channel story diverges from that of other channels. Numerous channels have been characterized, purified, sequenced, and cloned in the years since the hair cell mechanotransduction channel was discovered. Yet the hearing field has been left spinning its wheels in a molecular biology ditch. Scientists are still working to culture the cells, and the molecular identity of the transduction channel remains a mystery.
There are a number of reasons. For one, the amount of channel protein is in such low abundance that no one has been able to isolate it. "The first night that I was visiting Jim Hudspeth's lab, some people showed me the frog sacculus preparation. I had nightmares, literally, of how little material there was," Gillespie says.
The frog is used as a model because of its large hair cells, but it has only a few thousand of these cells with 100 stereocilia per cell. Other animals (fish, mice, humans) have comparably small numbers of hair cells. On each stereocilium likely exists only one mechanotransduction channel. Compare that to the retina, which has six orders of magnitude more cone photoreceptors than hair cells, and each outer segment of the photoreceptor possesses millions of copies of rhodopsin. To purify the mechanotransduction channel from hair cells, scientists "would need hundreds of thousands of animals," says Corey, now at Harvard Medical School.
They'd also need a high-affinity ligand. Tetrodotoxin binds specifically to sodium channels, and the purification technique Numa and colleagues used pulls out proteins bound to the toxin. 3 For the mechanotransduction channel, "people were finding it was a nonselective cation channel," says Corne Kros at the University of Sussex, but no one yet has identified a specific channel blocker. In the 1990s Kros and his colleagues began examining a number of different molecules, in particular, amiloride and its derivatives. They found that amiloride could plug up the open transduction channel. 4 "We found [that the transduction channels] were very different from almost everything, apart from the stretch sensitive channel in frog oocytes," Kros says. Amiloride seemed like a promising channel blocker, but scientists in the field of hearing would come to realize that hair cells seem to have more of an affinity for false leads than for available ligands.
Several years later, using the fluorescent dye FM1-43, Kros found that amiloride and antibiotics can slip through the transduction channel. 5 Though Kros says he was probably wrong in his initial interpretation that amiloride was not passing through the channel, it was an exciting finding because of evidence that antibiotic use can lead to deafness in patients. "On the basis of that [finding], we think that the transduction channel has a much bigger pore than was initially presumed," Kros says.
Kros also determined that FM1-43 permanently blocks the transduction channel. But, the block was not enough to do what Numa and his colleagues had done with the sodium channel. "If you want to use a blocker to isolate a channel, you need high affinity in the nanomolar range to use it as a handle to pull the channel out. Even FM1-43 is not quite in that class."
Even as one way to identify the channel proved fruitless, other opportunities soon became apparent. In 1987, researchers found a new way to clone channels. They had found a mutant Drosophila whose legs shook when the fly was anesthetized with ether. These now well-known "shaker" flies had alterations in their potassium channel currents, and a team from the University of California, San Francisco, was able to use the mutations to identify the potassium channel gene. 6
That finding afforded a new way to find the mechanotransduction channel. "The mutant strategy, in principle, should work," says Corey. Dozens of hearing mutants or balance mutants have been found in flies, zebrafish, mice, and humans. In 2000, one such mutant in Drosophila, nompC, put the hearing field at the edge of its seat.
On a July afternoon, the lunchtime crowd empties out of a courtyard patched with sun and shade at Oregon Health and Science University (OHSU). Richard Walker finishes a quesadilla and recounts how he pulled nompC from the crowd of a genetic screen. Charles Zuker's laboratory at the University of California, San Diego, had screened flies for defects in mechanotransduction. The collection was relatively uncharacterized when Walker joined the lab as a postdoc, and as he began to scrutinize the flies electrophysiologically, a particularly interesting mutant with four alleles caught his attention. "These flies are completely uncoordinated," Walker says. "They flop around like a drunken sailor, and [the mutation] is actually lethal in adults."
In physiological examinations Walker found that one of the alleles had a transduction current that would adapt much faster than wild-type flies. "The other three alleles all had almost all the transduction current abolished. We put two and two together and said, "'that's probably an important gene.'"
It was not just an important gene, but also perhaps the gene for the mechanotransduction channel. Walker did positional cloning to identify the nompC gene, which is homologous to members of the transient receptor potential (TRP) channel family. 7 He and his colleagues titled a paper on their findings (cited 198 times): "A Drosophila mechanosensory transduction channel." Gillespie says the feeling was, "I think we found it." Walker says, "it was a pretty big deal. It was heralded as a definite step forward in understanding mechanotransduction."
But the excitement was short-lived: nompC isn't present in any mammals. Teresa Nicolson, also at OHSU, found the gene in zebrafish, but humans, mice, even other species of fish lack the gene. "It's a mystery why it disappeared in higher vertebrates," Nicolson says.
It's clear the nompC channel - which is also called the TRPN1 channel - is not the transduction channel in mammals, and it appears not to be the only channel in animals that do express it, since nompC null mutants still have a small transduction current. "NompC might be partly responsible for the transduction channel, but it doesn't explain the whole story because of the residual current," Nicolson says. Whatever is responsible for that current is still unknown, but it's possible that therein might be the answer to the mammalian transduction channel, says Walker.
While hair cell research has frustrated some researchers, it hasn't been all failures. Identities of the other components of the transduction apparatus have emerged over the years. Most recently, Gillespie, Ulrich Müller at the Scripps Research Institute, and their colleagues - in perhaps an uncommon instance of serendipity and relative ease in the hearing field - nailed down the identity of the tip link, the molecule that stretches between any two stereocilia and is thought to open the transduction channel gate.
Müller's lab had been working on cell-to-cell interactions at the time when other researchers, including Nicolson, began cloning genes from deafness mutants. One gene that emerged from the screens, cadherin 23, is an adhesion molecule that caught Müller's attention. "The properties were similar to what we knew about the biochemical features of the tip link," Müller says. Mechanotransduction was nearly gone in the mutants, and stereocilia were splayed rather than bundled together. While Müller's lab was not involved in hair cells at the time, he decided to pursue the research. He recruited a postdoc to pioneer hair cell research in his laboratory, and sure enough, cadherin 23 turned out to be a main component of the tip link. 8
While molecular biologists are teasing out the tip link and other proteins in the transduction apparatus, biophysicists are whittling away the channel's mysteries by uncovering some of its physical properties. "We're trying to create a fingerprint of what this native channel is like, so as we try to compare to candidate channels, we know whether we're right or wrong," says Tony Ricci at Stanford University.
Ricci has found that the channel has unique properties that don't commit it to any known family. The biophysical properties and structure are similar to a TRP channel and an amiloride-sensitive sodium channel (ENac), "but not specifically any one of them." The transduction channel is 60% permeable to calcium, similar to a cyclic nucleotide channel, but the conductance is different between them.
The pore is about 1.2 nm in diameter, with a vestibule on the outside that allows large molecules to enter. The structure might explain how large molecules such as amiloride and antibiotics can enter the stereocilium, but once inside, can't get back out. "Like a Trojan horse, they don't go out anymore and wreak havoc in [the] cell," says Kros.
Ricci says determining the properties of the channel has been "tricky, because a lot of properties associated with the channel might not be intrinsic to the channel . but might be part of other machinery" associated with the channel. For this same reason, many hair cell researchers doubt the ability to take advantage of another technique widely used in channel research: expression of the channel in frog oocytes. Oocyte expression is used to confirm properties of a channel in the absence of confounding cellular components, but in the transduction channel, the tip link and other machinery might be necessary for function. Gillespie says such challenges beg the question: "How do you really prove what you've got is right?"
After Walker and his colleagues suggested that the transduction channel might be a TRP channel based on their work on nompC, Corey took the approach of a biased genetic screen, scanning through all the roughly 30 mouse TRP channels to see if any matched the transduction channel. One candidate, TRPA1, possessed qualities essential for the transduction channel: It was expressed in hair cells right around the time, developmentally, when the cells become mechanically sensitive, and an antibody to the channel became bound to the tips of the stereocilia, where the channel is thought to be located. 9 Furthermore, inhibiting the function of the channel resulted in far less transduction current. "That was the strongest evidence we were really convinced by this," says Corey. (His paper describing this candidate channel was cited 47 times within a year of being published, and a total of 151 times.)
To get conclusive evidence, however, Corey and his team created a mouse with a large chunk of the channel excised. Corey and others thought that 2005 might have been the year of cornering the channel, but the knockout mouse data were disappointing: The animals could hear just fine. As he wrote in a 2006 review article, "In the past 10 years, a variety of candidates have appeared, only to disappear, wraith-like, in the clear light of further experiments." 10
Robert Fettiplace at the University of Cambridge says that of the TRP channels, only one, TRPP, has nearly identical size and calcium permeability to the transduction channel, 11 yet there's no evidence of its existence in hair cells. While TRP channels still remain a possibility, "it's as likely to be a TRP channel as it is not," says Ricci. "Personally, I don't think it is."
The possibility of identifying the transduction channel thrills researchers, not only because the hunt for this elusive molecule could finally come to a close, but also because so many research possibilities would open up with having the transduction channel in hand. "There are wonderful things we could do - find out how it's connected to the tip link, to the actin cytoskeleton," Corey says. Understanding how the channel fits in to the transduction apparatus and the stereocilia could help illuminate repair mechanisms, such as the restringing of tip links after hearing loss from a rock concert, and could help in determining why those repair mechanisms break down.
Moreover, knowing the sequence of the channel and its "friends" could lead to understanding perhaps some of the hundred forms of nonsyndromal deafness, says Hudspeth, now at Rockefeller University. "In the long run one of our goals is at least to understand that, and for those who wanted to be cured, to try to alleviate that," he adds. One of Hudspeth's major lines of research, how the ear amplifies sound, might also have something to do with the channel, and having the channel in hand could go a long way in resolving how the ear accomplishes amplification (see 12 If those cells turn out to be physiologically and structurally similar to hair cells in vivo, the culture could lend itself to RNAi experiments and provide material in greater abundance than ears.
Ulrich isn't the first to think of it. "A really obvious experiment is to do siRNA suppression of everything you can think of," Gillespie says. One of his postdocs spent years trying to design a culture for siRNA experiments, but the cells didn't stay healthy in culture and measuring mechanotransduction was not reliable. Still, Gillespie says it needs to be done, and he's willing to invest more of his laboratory in developing an assay. "Even though I said it's frustrating to do siRNA, in a way we've got to get that to work. We're not going to make [knockout] mice for 25 proteins."
Gillespie's other approach is biochemical: Take all the proteins in the hair cell and examine them with mass spectrometry, in what he calls shotgun proteomics - "sequence everything." The difficulty here is that the transduction channel will be one of the least abundant proteins in the mix, and there aren't many criteria for whittling down the candidates, except at least a transmembrane domain and some sort of intracellular domain.
But then what? In terms of convincing the field that a candidate is the real deal, "the standard will be extremely high, particularly because TRPA1 was such a good target . but the genetics didn't work out," says Ulrich. "Even a knockout is not good enough in my mind," Gillespie says, "because all it says is that [the] channel is essential for hair cells, not that it's the transduction channel." Gillespie is creating mice with mutations in various TRP channel candidates, which would allow it to be inhibited from outside the hair cell. Then, Gillespie can stimulate the hair cell and observe whether the inhibitor affects the transduction current.
Corey's laboratory at Harvard Medical School is filled with cutting-edge equipment: a new two-photon microscope to track calcium's movements into and out of cells, floating floors to cut down on vibrations, and a machine shop so lab members can make their own equipment. In one of the floating rooms, Corey points out a laser-equipped rig that can be used to manipulate tiny movements in stereocilia using optical tweezers. Corey wants the transduction channel to be identified so he can use this equipment to do the really interesting experiments, such as determining how the whole transduction apparatus is constructed and how the system has developed such remarkable sensitivity. "We hope to find the transduction channel, and move on."
How large are the inner ear hairs? - Biology
Maltese can be very energetic, despite this they still do well for apartment dwellers. They are relatively easy to train and enjoy a playful game of fetch. These intelligent dogs learn quickly, and pick up new tricks and behaviors easily. Characteristics include slightly rounded skulls, with a one-finger-wide dome and a black nose that is two finger widths long. The body is compact with the length equaling the height. The drop ears with long hair and very dark eyes, surrounded by darker skin pigmentation that is called a "halo", gives Maltese their expressive look. Their noses can fade and become pink or light brown in color. This is often referred to as a "winter nose" and many times will become black again with increased exposure to the sun.
The coat is long and silky and lacks an undercoat. The color is pure white and although cream or light lemon ears are permissible, they are not desirable. Some individuals may have curly or woolly hair, but this is outside the standard. The Maltese while growing may get curly fur. They are very cute. Adult Maltese range from roughly(1.4 to 3.0 kg, though breed standards, as a whole, call for weights between 1.8 to 3. kg. There are variations depending on which standard is being used many, like the American Kennel Club, call for a weight that is ideally less than 7 lb with between 4 and 6 lb preferred.
For all their diminutive size, Maltese seem to be without fear. In fact, many Maltese seem relatively indifferent to creatures/objects larger than themselves, which makes them very easy to socialize with other dogs, and even cats. They are always happy, cheerful, smart and do not like to get into trouble. They tend to get very lonely if the master is not with them and taken care of and it doesn't like being left out. This is because they were bred to be companion dogs and thrive on love and attention. They are extremely lively and playful, and even as a Maltese ages, his/her energy level and playful demeanor remain fairly constant and does not diminish much.
Maltese are very good with children and infants. Maltese can sometimes be snappy and mean. Maltese do not require much physical exercise, although they should be walked daily to reduce problem behavior. They enjoy running and are more inclined to play games of chase, rather than play with toys. Maltese can be snappy with littler children and should always be supervised when playing. Socializing at a young age will reduce this habit. They can be very demanding and, true to their nature as "lap dogs", love to cuddle and often seek this sort of attention. The Maltese is very active in the house, and, preferring enclosed spaces, does very well with small yards. For this reason the breed also does well with apartments and townhouses, and is a prized pet of urban dwellers. They are incredibly friendly dogs to people they know. With strangers they will make a high pitched bark but will quiet down if the person means no harm.
The hair cells that line the inner ear and take part in the process of hearing can be irreversibly damaged by excessive noise levels. Intense sound blasts can rupture the tympanic membrane and dislocate or fracture the small bones of the middle ear. Hearing loss that…
…higher types of ears, containing hair cells and supporting elements, is called the organ of Corti.
…each end organ are the hair cells, the detection units for both linear and angular acceleration. Extending from each hair cell are fine, hairlike cilia displacement of the cilia alters the electrical potential of the cell. Bending the cilia in one direction causes the cell membrane to depolarize, while hyperpolarization…
The sensory cells are called hair cells because of the hairlike cilia—stiff nonmotile stereocilia and flexible motile kinocilia—that project from their apical ends. The nerve fibres are from the superior, or vestibular, division of the vestibulocochlear nerve.
The sensory cells are called hair cells because of the hairlike cilia—stiff nonmotile stereocilia and flexible motile kinocilia—that project from their apical ends. The nerve fibres are from the superior, or vestibular, division of the vestibulocochlear nerve. They pierce the basement membrane and, depending on the type of hair cell,…
…depending on the type of hair cell, either end on the basal end of the cell or form a calyx, or cuplike structure, that surrounds it.
…increases both the number of hair cells stimulated and the rate at which they generate nerve impulses.
Each has an organ containing hair cells similar to those of the organ of Corti. The utricle and saccule each contain a macula, an organ consisting of a patch of hair cells covered by a gelatinous membrane containing particles of calcium carbonate, called otoliths. Motions of the head cause the…
…up, and stimulation of the hair cells no longer occurs until rotation suddenly stops, again circulating the endolymph. Whenever the hair cells are thus stimulated, one normally experiences a sensation of rotation in space. During rotation one exhibits reflex nystagmus (back-and-forth movement) of the eyes. Slow displacement of the eye…
This deflection stimulates the hair cells by bending their stereocilia in the opposite direction. German physiologist Friedrich Goltz formulated the “hydrostatic concept” in 1870 to explain the working of the semicircular canals. He postulated that the canals are stimulated by the weight of the fluid they contain, the pressure…
… and the cilia of the hair cells beneath it. The otolithic membrane is covered with a mass of minute crystals of calcite (otoconia), which add to the membrane’s weight and increase the shearing forces set up in response to a slight displacement when the head is tilted. The hair bundles…
…sensitive cell known as a hair cell. The outer surface of these cells contains an array of tiny hairlike processes, including a kinocilium (not present in mammals), which has a typical internal fibre skeleton, and stereocilia, which do not have fibre skeletons. Stereocilia decrease in size with distance from the…
) Sound receptors are sensitive hair cells or membranes that depolarize a sensory neuron when bent by the passage of a sound wave. Direct deformation of the dendritic membrane or release of transmitters by the hair cells fire the sensory neurons. Aside from a few insects, only vertebrates have organs…
…and the sensory cells (hair cells) are arranged in a row on a ridge (crista) of the ampullar wall. The crista is oriented at right angles to the plane of the canal, and the extended hairs of its sensory cells are imbedded in a jellylike cupula that reaches to…
Detection of angular acceleration: dynamic equilibrium
Because the three semicircular canals—superior, posterior, and horizontal—are positioned at right angles to one another, they are able to detect movements in three-dimensional space. When the head begins to rotate in any direction, the inertia of the endolymph causes it to lag behind, exerting pressure that deflects the cupula in the opposite direction. This deflection stimulates the hair cells by bending their stereocilia in the opposite direction. German physiologist Friedrich Goltz formulated the “ hydrostatic concept” in 1870 to explain the working of the semicircular canals. He postulated that the canals are stimulated by the weight of the fluid they contain, the pressure it exerts varying with the head position. In 1873 Austrian scientists Ernst Mach and Josef Breuer and Scottish chemist Crum Brown, working independently, proposed the “ hydrodynamic concept,” which held that head movements cause a flow of endolymph in the canals and that the canals are then stimulated by the fluid movements or pressure changes. German physiologist J.R. Ewald showed that the compression of the horizontal canal in a pigeon by a small pneumatic hammer causes endolymph movement toward the crista and turning of the head and eyes toward the opposite side. Decompression reverses both the direction of endolymph movement and the turning of the head and eyes. The hydrodynamic concept was proved correct by later investigators who followed the path of a droplet of oil that was injected into the semicircular canal of a live fish. At the start of rotation in the plane of the canal, the cupula was deflected in the direction opposite to that of the movement and then returned slowly to its resting position. At the end of rotation it was deflected again, this time in the same direction as the rotation, and then returned once more to its upright stationary position. These deflections resulted from the inertia of the endolymph, which lags behind at the start of rotation and continues its motion after the head has ceased to rotate. The slow return is a function of the elasticity of the cupula itself.
These opposing deflections of the cupula affect the vestibular nerve in different ways, which have been demonstrated in experiments involving the labyrinth removed from a cartilaginous fish. The labyrinth, which remained active for some time after its removal from the animal, was used to record vestibular nerve impulses arising from one of the ampullar cristae. When the labyrinth was at rest there was a slow, continuous, spontaneous discharge of nerve impulses, which was increased by rotation in one direction and decreased by rotation in the other. In other words, the level of excitation rose or fell depending on the direction of rotation.
The deflection of the cupula excites the hair cells by bending the cilia atop them: deflection in one direction depolarizes the cells deflection in the other direction hyperpolarizes them. Electron-microscopic studies have shown how this polarization occurs. The hair bundles in the cristae are oriented along the axis of each canal. For example, each hair cell of the horizontal canals has its kinocilium facing toward the utricle, whereas each hair cell of the superior canals has its kinocilium facing away from the utricle. In the horizontal canals, deflection of the cupula toward the utricle—i.e., bending of the stereocilia toward the kinocilium—depolarizes the hair cells and increases the rate of discharge. Deflection away from the utricle causes hyperpolarization and decreases the rate of discharge. In superior canals these effects are reversed.
The ears and the auditory cortex of the brain are used to perceive sound. The ear is composed of the outer ear, middle ear, and inner ear. Each section performs distinct functions that help transform vibrations into sound.
The outer ear is made of skin, cartilage, and bone. It is also the site of the opening to the ear canal. A structure called the eardrum (tympanic membrane) lies at the end of the ear canal. The eardrum separates the outer ear from the middle ear. The ear canal contains protective hairs and ear wax (cerumen).
The middle ear (tympanic cavity) lies behind the eardrum. The middle ear contains three small bones (ossicles) that transmit sound waves from the eardrum to the inner ear. The three bones are called the malleus, the incus, and the stapes. The Eustachian tube connects the middle ear to the back of the nose. The Eustachian tube maintains the appropriate pressure in the middle ear that is necessary to transfer sound waves.
The inner ear contains the structures necessary for hearing and balance. The cochlea is the spiral shaped cavity that turns vibrations into nerve impulses that the brain perceives as sound. The vestibule and semicircular canals contain receptors that relay information about position and movement to the brain. This information is used to maintain balance.
Image Source: MedicineNet, Inc.
Text References: "Anatomy and Physiology of the Ear." Stanford Children’s Health. "Anatomy of the Ear." University of California Irvine.
MATERIALS AND METHODS
Five species from three different genera (Melamphaes, Poromitra, and Scopelogadus) were studied (Table 1, Fig. 1). The specimens were collected along the Eastern Pacific coast of Central America on a deep-sea research cruise SO 173-2 aboard the FS Sonne from August 8-September 2, 2003. Two kinds of nets were used during the trawls: A Tucker trawl net with an opening area of 3 m 2 with a closing cod end controlled by a timer, and a rectangular mid-water net with an opening area of 8 m 2 . The trawls were taken at depths of 600–1,000 m in waters of 2,000–5,600 m depth. The area of the stations during the cruise covered 10–14°N and 87–93°W.
|Species name||Common Name||Depth Range||Maximal SL||SL Range||Number of Specimens|
|Melamphaes acanthomus (Ebeling, 1962 )||Slender bigscale||250–3,500 m||110 mm||85–110 mm||7|
|Melamphaes laeviceps (Ebeling, 1962 )||Bald bigscale||400–1,109 m||134 mm||82–93 mm||4|
|Poromitra crassiceps (Günther, 1878)||Crested bigscale||0–3,400 m||180 mm||37–140 mm||7|
|Poromitra oscitans (Ebeling, 1975 )||Yawning||800–5,320 m||82 mm||53–75 mm||3|
|Scopelogadus mizolepis bispinosus (Gilbert, 1915)||Twospine bigscale||300–3,385 m||94 mm||50–71 mm||8|
Fishes were dead by the time they were brought to the surface (approximately one hour). The catches were taken onto the deck and collected in trays containing cold seawater. Photographs of fishes were taken before they were handled (Fig. 1), and morphological data for species identification were recorded. The number of specimens used in this study and the size range are shown in Table 1. Since the tissue used was not collected directly for this project, and since the animals were already dead when made available for investigation, the University of Maryland Animal Care and Use Committee indicated that no animal use protocol was required for this study.
The species were identified using a variety of sources (Ebeling, 1962, 1975 Ebeling and Weed, 1963 Carpenter, 2002 Kotlyar, 2004, 2008a, 2008b , 2009 Smale et al., 1995 ) and confirmed by the otolith collection (isolated from fresh specimens and air-dried) at the Scripps Institution of Oceanography (SIO 64-12, SIO 64-13, SIO 67-52, and SIO 68-52, http://collections.ucsd.edu/mv/fish_collection/otoliths.html). The geographic distributions of these species at collecting locations were confirmed by the database at Global Biodiversity Information Facility (GBIF, http://data.gbif.org/welcome.htm).
The specimens were fixed in cold 4% paraformaldehyde and 2% glutaraldehyde in 0.1 M cacodylate buffer with 0.05% CaCl2 and 0.1 M sucrose. Small specimens were fixed whole while for the bigger specimens, heads were trimmed, and the skull roofs were opened to ensure fast fixative penetration. In addition, some fishes were dissected on board immediately after coming to the surface and then photographed to obtain the structure of the otolith and otolith membrane before being exposed to any effects of fixation. After returning to the lab at the University of Maryland, the fixative was replaced with 0.1 M cacodylate buffer with 0.05% CaCl2 and 0.1 M sucrose and the specimens were stored in a 4°C refrigerator until further analysis.
Inner ears were photographed during dissections while they were immersed in buffer. The tissues were then post fixed in 1% OsO4 with 0.1 M cacodylate buffer at room temperature for 30–60 min. After one buffer rinse followed by three double distilled water rinses, the tissues were dehydrated for 10 min each in 30%, 50%, 75%, 85%, 95%, and 3 ×100% ethanol. Critical point drying was carried out using CO2 as the intermediary fluid. The end organ tissues were then mounted on aluminum stubs and coated with a 6–12 nm thick layer of Au-Pt in a Denton Vacuum DV 503, and viewed with an AMRAY 1820D scanning electron microscope (SEM).
SEM analyses included determination of the hair bundles' direction of sensitivity, as defined by the side of the bundle at which the kinocilium located, and measurement of their height. The relative measurements of hair bundle height were taken using a SEM Digital Imaging System provided by SEMtech Solutions INC during the operations on AMRAY 1820D, as well as on SEM images. Measurements of very high bundles were sampled from those that were stretched out on the surface of the epithelium, whereas measurements of low, standing bundles were taken by tilting the SEM stub so that the bundles were parallel to the viewing plane in order to prevent the effects of foreshadowing in SEM images. All measurements are relative because of shrinkage of samples during dehydration and the tilting and bending of hair bundles.
Gross morphology pictures were taken using a digital camera and a dissecting stereomicroscope on a dark background. Only minimal digital manipulations were made using Adobe Photoshop 7.0 in order to prepare the figures for publication. The manipulations were limited to adjusting brightness and contrast and occasional adjustment of the color balance to eliminate lighting artifacts.
A molecular phylogeny of Melamphaidae was constructed using DNA sequences of the widely used mitochondrial gene, cytochrome c oxidase subunit I (mtCOI). All DNA sequences were obtained from GenBank (Table 2). The phylogenetic tree was built using the maximum likelihood method with a best-fit DNA substitution model (TIM2+I+G) selected by jModeltest v0.1.1 (Posada 2008 ). Two Beryx species from Berycidae were used as an outgroup to root the tree and resolve the cladogenesis within Melamphaidae.
|Taxon name||GenBank Accession number|
|P. crassiceps||FJ165049, HQ713196|
- DNA sequences of the mitochondrial gene, cytochrome c oxidase, were selected from key taxonomic groups within the family Melamphaidae, representing the genetic diversity within species and genus. Two sequences from Berycidae were included as outgroup.
Bring in the Sound
Now, let’s get back to those air molecules. When the air molecules reach your ear, they travel through your ear canal until they bump into your eardrum.
The movement of sound waves can be thought of in a similar way to the game pieces of Dominoes. Click for more detail.
Have you ever played with dominoes? You line them all up and push against the first one. This domino falls into the next one, making it fall into the next one, and so on. Sound works the same way. Every time sound hits something, it makes something else move. This is how sound moves down the pathway to get to your brain.
The air molecules moving through your ear canal cause the eardrum to move back and forth. The middle ear bones are connected to your eardrum and start moving back and forth too.
The back and forth motion of the bones pushes on a membrane of the cochlea called the oval window. Because the bones are pushing on the oval window, fluid starts moving back and forth inside the cochlea. When the fluid is moving, it moves tiny little cells called hair cells lined up inside the cochlea.
It's almost like sea grass being moved by the current. When fluid pushes on the hair cells, they are activated and send a neural signal to the auditory nerve. Signals travel through this nerve to your brain so that you can understand the message.
Promoting good ear health
Once hearing is gone, it is impossible to repair it naturally. Most patients with hearing loss need surgery or hearing aids. "The good news is that this is 100 percent preventable," said Cherukuri. "I tell my patients to follow the 60-60 rule when they use earbuds or headphones: No more than 60 percent of full volume for no longer than 60 minutes at a time."
People who participate in noisy activities or hobbies, such as sporting events, music concerts, shooting sports, motorcycle riding or mowing the lawn, should also wear earplugs or noise-canceling or noise-blocking headphones to help protect the ears.
Careful cleaning is another way to prevent hearing loss and damage. The American Academy of Otolaryngology suggests cleaning the external ear with a cloth. Then, put a few drops of mineral oil, baby oil, glycerin, or commercial drops in the ear to soften the wax and help it drain out of the ear. A few drops of hydrogen peroxide or carbamide peroxide may also help. Never insert anything into the ear.
Editor&rsquos Note: If you&rsquod like more information on this topic, we recommend the following book: