The cochlea pron.: /kk.l/ is the auditory portion of the inner ear.

It is a spiral-shaped cavity in [1] the bony labyrinth, in humans making 2.5 turns around its axis, the modiolus. A core component of the cochlea is the Organ of Corti, the sensory organ ofhearing, which is distributed along the partition separating fluid chambers in the coiled tapered tube of the cochlea. The name is derived from the Latin for snail shell, which in turn is from the Greek kokhlias ("snail, [2] screw"), from kokhlos ("spiral shell") in reference to its coiled shape; the cochlea is coiled in mammals with the exception of monotremes.

Anatomy

Structures
The cochlea (plural is cochleae) is a spiralled, hollow, conical chamber of bone, in which waves propagate from the base (near the middle ear and the oval window) to the apex (the top or center of the spiral). Its structures include: Three scalae or chambers: the scala vestibuli (containing perilymph), which lies superior to the cochlear duct and abuts the oval window the scala tympani (containing perilymph), which lies inferior to the scala media and terminates at the round window the scala media (containing endolymph), or cochlear duct, a region of high potassium ion concentration that the stereocilia of the hair cells project into The helicotrema, the location where the scala tympani and the scala vestibuli merge, at the apex of the cochlea Reissner's membrane, which separates the scala vestibuli from the scala media The basilar membrane, a main structural element that separates the scala media from the scala tympani and determines the mechanical wave propagation properties of the cochlear partition The Organ of Corti, the sensory epithelium, a cellular layer on the basilar membrane, in which sensory hair cells are powered by the potential difference between the perilymph and the endolymph hair cells, sensory cells in the Organ of Corti, topped with hair-like structures called stereocilia or (more properly) stereovilli.

The cochlea is a portion of the inner ear that looks like a snail shell (cochlea is Latin for snail.) The cochlea receives sound in the form of vibrations, which cause the stereocilia to move. The stereocilia then convert these vibrations into nerve impulses which are taken up to the brain to be interpreted. Two of the three fluid sections are canals and the third is a sensitive 'organ of Corti' which detects pressure impulses which travel along the auditory nerve to the brain. The two canals are called the vestibular canal and the tympanic canal. [edit]Detailed

anatomy

The walls of the hollow cochlea are made of bone, with a thin, delicate lining of epithelial tissue. This coiled tube is divided through most of its length by an inner membranous partition. Two fluid-filled outer

spaces (scalae) are formed by this dividing membrane. At the top of the snailshell-like coiling tubes, there is a reversal of the direction of the fluid, thus changing the scala vestibuli to the scala tympani. This area is called the helicotrema. This continuation at the helicotrema allows fluid being pushed into the scala vestibuli by the oval window to move back out via movement in scala tympani and deflection of the round window; since the fluid is nearly incompressible and the bony walls are rigid, it is essential for the conserved fluid volume to exit somewhere. The lengthwise partition that divides most of the cochlea is itself a fluid-filled tube, the third scala. This central column is called the scala media, or cochlear duct. Its fluid,endolymph, also contains electrolytes and proteins, but is chemically quite different from perilymph. Whereas the perilymph is rich in sodium ions, the endolymph is rich in potassium ions, which produces an ionic, electrical potential. The hair cells are arranged in four rows in the organ of Corti along the entire length of the cochlear coil. Three rows consist of outer hair cells (OHCs) and one row consists of inner hair cells (IHCs). The inner hair cells provide the main neural output of the cochlea. The outer hair cells, instead, mainly receive neural input from the brain, which influences their motility as part of the cochlea's mechanical pre-amplifier. The input to the OHC is from the olivary body via the medial olivocochlear bundle. The cochlear duct is almost as complex on its own as the ear itself. The cochlear duct is bounded on three sides by the basilar membrane, the stria vascularis, and Reissner's membrane. Stria vascularis is a rich bed of capillaries and secretory cells; Reissner's membrane is a thin membrane that separates endolymph from perilymph; and the basilar membrane is a mechanically somewhat stiff membrane, supporting the receptor organ for hearing, the organ of Corti, and determines the mechanical wave propagration properties of the cochlear system. [edit]Physiological [edit]Summary The cochlea is filled with a watery liquid, the perilymph, which moves in response to the vibrations coming from the middle ear via the oval window. As the fluid moves, the cochlear partition (basilar membrane and organ of Corti) moves; thousands of hair cells sense the motion via their stereocilia, and convert that motion to electrical signals that are communicated via neurotransmitters to many thousands of nerve cells. These primary auditory neurons transform the signals into electrochemical impulses known as action potentials, which travel along the auditory nerve to structures in the brainstem for further processing.

functioning

[edit]Detailed

events

The stapes (stirrup) ossicle bone of the middle ear transmits vibrations to the fenestra ovalis (oval window) on the outside of the cochlea, which vibrates the perilymph in the scala vestibuli (upper chamber of the cochlea). The ossicles are essential for efficient coupling of sound waves into the cochlea, since the cochlea environment is a fluidmembrane system, and it takes more pressure to move sound through fluidmembrane waves than it does through air; a pressure increase is achieved by the area ratio of the tympanic membrane to the oval window, resulting in a pressure gain of about 20 from the original sound wave pressure in air. This gain is a form of impedance matching to match the soundwave travelling through air to that travelling in the fluidmembrane system. At the base of the cochlea, each scala ends in a membranous portal that faces the middle ear cavity: The scala vestibuli ends at the oval window, where the footplate of the stapes sits. The footplate vibrates when the pressure is transmitted via the ossicular chain. The wave in the perilymph moves away from the footplate and towards the helicotrema. Since those fluid waves move the cochlear partition that separates the scalae up and down, the waves have a corresponding symmetric part in perilymph of the scala tympani, which ends at the round window, bulging out when the oval window bulges in.

The perilymph in scala vestibuli and the endolymph in scala media act mechanically as a single duct, being kept apart only by the very thin Reissner's membrane. The vibrations of the endolymph in the scala media displace the basilar membrane in a pattern that peaks a distance from the oval window depending upon the soundwave frequency. The organ of Corti vibrates due to outer hair cells further amplifying these vibrations. Inner hair cells are then displaced by the vibrations in the fluid, and depolarise by an influx of K+ via their tip-link-connected channels, and send their signals via neurotransmitter to the primary auditory neurons of the spiral ganglion. The hair cells in the organ of Corti are tuned to certain sound frequencies by way of their location in the [3] cochlea, due to the degree of stiffness in the basilar membrane. This stiffness is due to, among other [4] things, the thickness and width of the basilar membrane, which along the length of the cochlea is stiffest nearest its beginning at the oval window, where the stapes introduces the vibrations coming from the eardrum. Since its stiffness is high there, it allows only high-frequency vibrations to move the basilar membrane, and thus the hair cells. The farther a wave travels towards the cochlea's apex (the helicotrema), the less stiff the basilar membrane is; thus lower frequencies travel down the tube, and the less-stiff membrane is moved most easily by them where the reduced stiffness allows: that is, as the basilar membrane gets less and less stiff, waves slow down and it responds better to lower frequencies. In addition, in mammals, the cochlea is coiled, which has been shown to enhance low-frequency [5] vibrations as they travel through the fluid-filled coil. This spatial arrangement of sound reception is referred to as tonotopy. For very low frequencies (below 20 Hz), the waves propagate along the complete route of the cochlea differentially up scala vestibuli and scala tympani all the way to thehelicotrema. Frequencies this low still activate the organ of Corti to some extent, but are too low to elicit the perception of a pitch. Higher frequencies do not propagate to thehelicotrema, due to the stiffness-mediated tonotopy. A very strong movement of the basilar membrane due to very loud noise may cause hair cells to die. This is a common cause of partial hearing loss and is the reason why users of firearms or heavy machinery often wear earmuffs or earplugs. [edit]Phenomena [edit]Amplification

by the hair cells

Not only does the cochlea "receive" sound, it generates and amplifies sound when it is healthy. Where the organism needs a mechanism to hear very faint sounds, the cochlea amplifies by the reverse transduction of the OHCs, converting electrical signals back to mechanical in a positive-feedback configuration. The OHCs have a protein motor calledprestin on their outer membranes; it generates additional movement that couples back to the fluidmembrane wave. This "active amplifier" is essential in the ear's ability to amplify weak sounds. The active amplifier also leads to the phenomenon of soundwave vibrations being emitted from the cochlea back into the ear canal through the middle ear (otoacoustic emissions). [edit]Otoacoustic

emissions

Otoacoustic emissions are due to a wave exiting the cochlea via the oval window, and propagating back through the middle ear to the eardrum, and out the ear canal, where it can be picked up by a microphone. Otoacoustic emissions are important in some types of tests for hearing impairment, since they are present when the cochlea is working well, and less so when it is suffering from loss of OHC activity. [edit]Comparative

physiology

The coiled form of cochlea is unique to mammals. In birds and in other non-mammalian vertebrates, the compartment containing the sensory cells for hearing is occasionally also called "cochlea," despite not

being coiled up. Instead, it forms a blind-ended tube, also called the cochlear duct. This difference apparently evolved in parallel with the differences infrequency range of hearing and in frequency resolution between mammals and non-mammalian vertebrates. Most bird species do not hear above 4 5 kHz, the currently known maximum being ~ 11 kHz in the barn owl. Some marine mammals hear up to 200 kHz. The superior frequency resolution in mammals is due to their unique mechanism of preamplification of sound by active cell-body vibrations of outer hair cells. A long coiled compartment, rather than a short and straight one, provides more space for mapping pitches, so is therefore better adapted to [6] the highly derived functions in mammalian hearing. As the study of the cochlea should fundamentally be focused at the level of hair cells, it is important to note the anatomical and physiological differences between the hair cells of various species. In birds, for instance, instead of outer and inner hair cells, there are tall and short hair cells. There are several similarities of note in regard to this comparative data. For one, the tall hair cell is very similar in function to that of the inner hair cell, and the short hair cell is very similar in function to that of the outer hair cell. One unavoidable difference, however, is that while all hair cells are attached to a tectorial membrane in birds, only the outer hair cells are attached to the tectorial membrane in mammals.

Organ of Corti
The organ of Corti, found only in mammals, is part of the cochlea of the inner ear and is provided [1] with hair cells or auditory sensory cells. It evolved from the basilar papilla found in all tetrapods, except [2] for a few derived species that have lost it. The organ was named after the Italian anatomist Marquis Alfonso Giacomo Gaspare Corti (18221876), who conducted microscopic research of the mammalian auditory system.

Structure and functions

The organ of Corti has highly specialized structures that respond to fluid-borne vibrations in the cochlea with a shearing vector in the hairs of some cochlear hair cells. It contains between 15,00020,000 auditory nerve receptors. Each receptor has its own hair cell. The shear on the hairs opens nonselective transduction ion channels that are permeable to potassium and calcium, leading to hair cell plasma membrane depolarization, activation of voltage-dependent calcium channels at the synaptic basolateral pole of the cells which triggers vesicle exocytosis and liberation of glutamate neurotransmitter to the synaptic cleft and electrical signaling to the auditory cortex via spiral ganglion neurons. The pinna and middle ear act as mechanical transformers and amplifiers, so that by the time sound

waves reach the organ of Corti, their pressure amplitude is 22 times that of the air impinging on the pinna. The organ of Corti can be damaged by excessive sound levels, leading tonoise-induced health effects. The organ of Corti is the structure that transduces pressure waves to action potentials. The organ of Corti sits inside the cochlear duct, between the scala vestibuli and the scala tympani. The basilar membrane on the scala tympani presses against the hair cells of the organ as perilymphatic pressure waves pass.

Cochlear amplifier
From Wikipedia, the free encyclopedia

The cochlear amplifier is a positive feedback mechanism within the cochlea that provides acute sensitivity in the mammalian auditory system.[1] The main component of the cochlear amplifier is the outer hair cell (OHC) which increases the amplitude and frequency selectivity of sound vibrations using electromechanical feedback.[2]
Contents
[hide]

1 Discovery 2 Function

o o o

2.1 Effect of sound waves on the cochlea 2.2 The somatic motor 2.3 The hair bundle motor

2.3.1 Fast adaptation 2.3.2 Slow adaptation

2.4 Integration of electromotility and hair bundle dynamics

3 References

[edit]Discovery
The cochlear amplifier was first proposed in 1948 by T. Gold.[3] This was around the time when Georg von Bksy was publishing articles observing the propagation of passive travelling waves in the dead cochlea. Thirty years later the first recordings of emissions from the ear were captured by D.T. Kemp. [4] This was confirmation that such an active mechanism was present in the ear. These emissions are now termed otoacoustic emissions and are produced by what we call the cochlear amplifier. The first modeling effort to define the cochlear amplifier was a simple augmentation of Georg von Bksy's passive traveling wave with an active component. In such a model, a lop sided pressure about the Organ of Corti is hypothesized which actively adds to the passive traveling wave to form the active traveling wave. Perhaps the most popular example of this model was defined by Neely, S.T. and Kim, D.O.[5] The definition of the active traveling waves require forward and backward traveling waves to be generated in the cochlea, as proposed by Shera, C.A. and Guinan, J.J.[6]

Contention still surrounds the existence of the active traveling wave. Recent experiments conducted by T. Ren[7] show that emissions from the ear occur with such a fast response that the slowly propagating active traveling waves can not exist. The only explanation for fast emission propagation is the dual of the active traveling wave, the active compression wave. Active compression waves were proposed as early as 1980 by P.J. Wilson[8] due to older experimental data. However, they were widely disregarded by the research community until stronger experimental proof confirming these early experiments against the active traveling wave was produced. Thirty years after Kemp's experimental proof of the existence of Gold's cochlear amplifier and sixty years after the proposal of Gold's cochlear amplifier, the active-compression-wave cochlear amplifier was defined by M.R. Flax and W.H. Holmes.[9][10] In this model the active pressure is equal on both sides of the Organ of Corti and this produces very fast propagating pressure waves which generate extra activity within the cochlea and emissions through the middle/outer ear. This original OHC compression model was taken further to explain a 'mixed mode' cochlear amplifier in 2011, where the apex and base of the cochlea are modelled by the same system proposed by Flax and Holmes,[11] however experimentally capture different modes of stimulation as proposed by Guinan.[12] Other explanations for the active processes in the inner ear exist[13][14][15] however these explanations are not as popular and old as the active-traveling-wave and active-compression-wave cochlear amplifier models.

[edit]Function [edit]Effect

of sound waves on the cochlea

In the mammalian cochlea, amplification occurs in the outer hair cells of the Organ of Corti. These cells sit directly above a basilar membrane (BM) that has high sensitivity for differences in frequency. Sound waves enter the scala vestibuli of the cochlear and travel throughout it, carrying with them various sound frequencies. These waves exert a pressure on the basilar and tectorial membranes of the cochlea which vibrate in response to sound waves of different frequencies. When these membranes vibrate and are deflected upward (rarefaction phase of sound wave), the stereocilia of the OHCs are deflected toward the tallest stereocilia. This causes the tip links of the OHC hair bundle to open allowing inflow of Na+ and K+ which depolarize the OHC. Upon depolarization, the OHC can then begin its process of amplification through positive feedback. This positive feedback mechanism is achieved through a somatic motor and a hair bundle motor which operate independently of one another.

[edit]The

somatic motor

The somatic motor is the OHC cell body and its ability to elongate or contract longitudinally due to changes in membrane potential. This function is aptly associated with the OHC structure within the Organ of Corti. As seen through scanning electron micrograph imagery, the apical side of the OHC is mechanically coupled to the reticular lamina while the basal side of the OHC is coupled to the Deiter's cell cupula. [16] Because the cell body is not in direct contact with any structure and is surrounded by the fluid-like endolymph, the OHC is considered dynamic and able to support electromotility.

Prestin is the transmembrane protein underlying the OHC's ability to elongate and contract, a process essential for OHC electromotility. This protein is voltage-sensitive. Contrary to previous research, prestin has also been shown to transport anions; the exact role of anion-transport in the somatic motor is still under investigation.[17] Under resting conditions, it is thought that chloride is bound to allosteric sites in prestin. Upon deflection of the BM upwards and subsequent deflection of the hair bundles toward the tallest steroecilia, channels within the stereocilia open allowing the inflow of ions and depolarizing the OHC results. Intracellular chloride dissociates from the allosteric binding sites in prestin, causing contraction of prestin. Upon BM deflection downwards hyperpolarization of the OHC results, and intracellular chloride ions bind allosterically causing prestin expansion.[18] The binding or dissociation of chloride causes a shift in prestin's membrane capacitance. A nonlinear capacitance (NLC) results which leads to a voltage-induced mechanical displacement of prestin into an elongated or contracted state as described above. The larger the voltage nonlinearity, the larger prestin's response; this shows a concentration specific voltage-sensitivity of prestin. Prestin densely lines the lipid bilayer of the outer hair cell membranes.[17][18] Therefore, a change in the shape of many prestin proteins, which tend to conglomerate together, will ultimately lead to a change in shape of the OHC. A lengthening of prestin lengthens the hair cell while prestin contraction leads to a decrease in OHC length.[18] Because the OHC is tightly associated with the reticular lamina and the Deiter's cell, shape change of the OHC leads to movement of these upper and lower membranes, causing changes in vibrations detected in the cochlear partition. Upon initial deflection of the BM causing positive hair bundle deflection, the reticular lamina is pushed downward, resulting in a negative deflection of the hair bundles. This causes stereocilia channel closing which leads to hyperpolarization and OHC elongation.[19] Below the hair bundle is an actin-rich cuticular plate.[16] It has been hypothesized that the role of actin depolymerization is crucial for regulation of the cochlear amplifier. Upon actin polymerization, electromotile amplitude and OHC length increase.[1] These changes in actin polymerization do not alter NLC, showing that actin's role in the cochlear amplifier is separate from that of prestin.

[edit]The

hair bundle motor

The hair bundle motor is the force generated from a mechanical stimulus. This is done through the use of the mechanoelectrical transduction (MET) channel, which allows for the passage of Na+, K+, and Ca2+.[20] The hair bundle motor operates by deflecting hair bundles in the positive direction and providing positive feedback of the basilar membrane, increasing the movement of the basilar membrane which increases the response to a signal. Two mechanisms have been proposed for this motor: fast adaptation, or channel re-closure, and slow adaptation.

[edit]Fast adaptation
This model relies upon a calcium gradient generated by the opening and closing of the MET channel. Positive deflection of the tip links stretches them in the direction of the tallest stereocilia, causing MET channel opening. This allows the passage of Na+, K+, and Ca2+.[21] Additionally, Ca2+ briefly binds to a cytostolic site on the MET channel which is estimated to be only 5 nm from the channel pore. Because of close proximity to the channel opening, it is suspected that Ca2+ binding affinty can be relatively low. When calcium binds to this site, the MET

channels begin to close. Channel closure ceases the transduction current and increases the tension in the tip links, forcing them back in the negative direction of the stimulus. Binding of calcium is short-lived, because the MET channel must participate in additional cycles of amplification. When calcium dissociates from the binding site, calcium levels fall rapidly. Due to the differences in calcium concentration at the cytostolic binding site when calcium is bound to the MET channel versus when calcium dissocates, a calcium gradient is created, generating chemical energy. The oscillation of calcium concentration and force generation contributes to amplification.[21][22] The timecourse of this mechanism is on the order of hundreds of microseconds, which reflects the speed that is necessary for amplification of high frequencies.

[edit]Slow adaptation
As oppose to the fast adaptation model, slow adaptation relies on the myosin motor to alter the stiffness of the tip links leading to alterations of channel current. First, the stereocilia are deflected in the positive direction opening the MET channels and allowing for inflow of Na+, K+, and Ca2+. The entering current first increases and then quickly decreases due to myosin's release of tension of the tip link and subsequent closing of channels.[23] It is hypothesized that the tip link is attached to the myosin motor which moves along actin filaments.[24] Again the polymerization of actin could play a crucial role in this mechanism, as it does in OHC electromotility. Calcium has also been shown to play a crucial role in this mechanism. Experiments have shown that in reduced extracellular calcium, the myosin motor tightens, resulting in more open channels. Then, when additional channels are opened, the inflow of calcium acts to relax the myosin motor, which returns the tip links to their resting state, causing channels to close.[23] This is hypothesized to occur via the binding of calcium to the myosin motor. The timecourse of this event is 10-20 milliseconds. This time scale reflects the time that is needed to amplify low frequencies.[22] Although the largest contributor to slow adaptation is the tensiondependence, calcium-dependence acts as a useful feedback mechanism. This mechanism of myosin's reaction to hair bundle deflection imparts sensitivity to small changes in hair bundle position.

[edit]Integration

of electromotility and hair bundle dynamics

Electromotility of the OHC by prestin modulation produces significantly larger forces than the forces generated by deflection of the hair bundle. One experiment showed that the somatic motor produced a 40-fold greater force at the apical membrane and a sixfold greater force at the basilar membrane than the hair bundle motor. The difference in these two motors is that there are different polarities of hair bundle deflection for each motor. The hair bundle motor uses a positive deflection leading to a generation of force, while the somatic motor uses negative deflection to generate force. However, both the somatic motor and the hair bundle motor produce significant displacements of the basilar membrane. This, in turn, leads to augmentation of bundle movement and signal amplification.[19] The mechanical force that is generated by these mechanisms increases the movement of the basilar membrane. This, in turn, influences the deflection of the hair bundles of the inner hair cells. These cells are in contact with afferent fibers that are responsible for transmitting signals to the brain.

Georg von Bksy

From Wikipedia, the free encyclopedia

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The native form of this personal name is Bksy Gyrgy. This article uses the Western name order.

Georg von Bksy

Bksy won a Nobel Prize in 1961

Born

3 June 1899 Budapest, Hungary

Died

13 June 1972 (aged 73) Honolulu, Hawaii, United States

Nationality

Hungarian

Fields

Biophysics

Known for

Cochlea

Notable awards

Nobel Prize in Physiology or Medicine (1961)

Georg von Bksy (Bksy Gyrgy) (June 3, 1899 June 13, 1972) was a Hungarian biophysicist born in Budapest, Hungary. In 1961, he was awarded the Nobel Prize in Physiology or Medicine for his research on the function of the cochlea in the mammalian hearing organ.
Contents
[hide]

1 Biography 2 Research 3 Awards 4 References 5 Further reading 6 External links

[edit]Biography
Bksy was born on June 3, 1899 in Budapest, Hungary, the first of three children (Gyrgy 1899, Lola 1901 and Mikls 1903) to Alexander von Bksy (18601923), an economic diplomat born in Kolozsvr, Transylvania, Kingdom of Hungary, and his wife Paula Mazaly (18791974) born in Cadavica, Slavonia, Kingdom of Hungary. He went to school in Budapest, Munich, and Zrich. He studiedchemistry in Bern and received his PhD in physics on the subject: "Fast way of determining molecular weight" from the University of Budapest in 1926. He then spent one year working in an engineering firm. He published his first paper on the pattern of vibrations of the inner ear in 1928. He was offered a position at Uppsala University by Rbert Brny, which he dismissed because of the hard Swedish winters. Before and during World War II, Bksy worked for the Hungarian Post Office (1923 to 1946), where he did research on telecommunications signal quality. This research led him to become interested in the workings of the ear. In 1946, he left Hungary to follow this line of research at the Karolinska Institute in Sweden. In 1947, he moved to the United States, working at Harvard University until 1966. After his lab was destroyed by fire in 1965, he was offered to lead a research laboratory of sense organs in Honolulu, Hawaii. He became a professor at the University of Hawaii in 1966 and died in Honolulu. He became a well-known expert in Asian art. He had a large collection which he donated to the Nobel Foundation in Sweden. His brother, Dr. Mikls Bksy (born 1903), stayed in Hungary and became a famous agrobiologist who was awarded the Kossuth Prize.

[edit]Research
Bksy developed a method for dissecting the inner ear of human cadavers while leaving the cochlea partly intact. By using strobe photography and silver flakes as a marker, he was able to observe that the basilar membrane moves like a surface wave when stimulated by sound. Because of the structure of the cochlea and the basilar membrane, differentfrequencies of sound cause the maximum amplitudes of the waves to occur at

different places on the basilar membrane along the coil of the cochlea.[1] High frequencies cause more vibration at the base of the cochlea while low frequencies create more vibration at the apex.[2] He concluded that his observations showed how different sound wave frequencies are locally dispersed before exciting different nerve fibers that lead from the cochlea to the brain. He theorized that the placement of each sensory cell (hair cell) along the coil of the cochlea corresponds to a specific frequency of sound (the socalled tonotopy). Bksy later developed a mechanical model of the cochlea, which confirmed the concept of frequency dispersion by the basilar membrane in the mammalian cochlea. But this model could not provide any information as to a possible function of this frequency dispersion in the process of hearing. [1] In a posthumous 1974 article looking back over progress in the field, he remarked "In time, I came to the conclusion that the dehydrated cats and the application of Fourier analysisto hearing problems became more and more a handicap for research in hearing,"[3] referring to the difficulties in getting animal preparations to behave as when alive, and the misleading common interpretations of Fourier analysis in hearing research.

[edit]Awards
Bksy's honours include:

The Denker Prize in Otology (1931), The Leibnitz Medal of the Berlin Academy of Sciences (1937), The Guyot Prize for Speech and Otology of Groningen University (1939), The Academy Award of the Budapest Academy of Science (1946), Shambough Prize in Otology (1950).

Honorary doctorates (M.D.) were conferred on him by the University of Munster (1955), Bern (1959), Padua (1962), Buenos Aires (1968), Cordoba (1968), Hawaii (1969) and Semmelweiss University, Budapest (1969).

Tonotopy
From Wikipedia, the free encyclopedia

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In physiology, tonotopy (from Greek tono- and topos = place) is the spatial arrangement of where sounds of different frequency are processed in the brain. Tones close to each other in terms of frequency are represented in topologically neighbouring regions in the brain. Tonotopic maps are a particular case of topographic organization, similar to retinotopyin the visual system. Tonotopy in the auditory system begins at the cochlea, the small snail-like structure in the inner ear that sends information about sound to the brain. Different regions of the basilar membrane in the organ of Corti, the sound-sensitive portion of the cochlea, vibrate at different sinusoidal frequencies due to variations in thickness and width along the length of the membrane. Nerves that transmit information from different regions of the basilar membrane therefore encode frequency tonotopically. This tonotopy then projects through thevestibulocochlear nerve and associated midbrain structures to the primary auditory cortex via the auditory

radiation pathway. Throughout this radiation, organization is linear with relation to placement on the organ of Corti, in accordance to the best frequency response (that is, the frequency at which that neuron is most sensitive) of each neuron. However,binaural fusion in the superior oliviary complex onward adds significant amounts of information encoded in the signal strength of each ganglion. Thus, the number of tonotopic maps varies between species and the degree of binaural synthesis and separation of sound intensities; in humans, six tonotopic maps have been identified in the primary auditory cortex.[1] These maps can be generalized by their anatomical locations along the auditory cortex.

sounds of low pitch project into the anterolateral aspect of Heschl's gyrus sounds of high pitch project deeply into the lateral fissure (which houses Heschl's gyrus

Place theory (hearing)

From Wikipedia, the free encyclopedia

Place theory is a theory of hearing which states that our perception of sound depends on where each component frequency produces vibrations along the basilar membrane. By this theory, the pitch of a musical tone is determined by the places where the membrane vibrates, based on frequencies corresponding to the tonotopic organization of the primary auditory neurons.[1][2] More generally, schemes that base attributes of auditory perception on the neural firing rate as a function of place are known as rateplace schemes.[3] The main alternative to the place theory is the temporal theory,[2] also known as timing theory.[1] These theories are closely linked with the volley principle or volley theory,[4] a mechanism by which groups of neurons can encode the timing of a sound waveform. In all cases, neural firing patterns in time determine the perception of pitch. The combination known as the placevolley theory uses both mechanisms in combination, primarily coding low pitches by temporal pattern and high pitches by rateplace patterns.[4] It is now generally believed that there is good evidence for both mechanisms.[5] The place theory is usually attributed to Hermann Helmholtz, though it was widely believed much earlier.[6][7] Experiments to distinguish between place theory and rate theory are difficult to devise, because of the strong correlation: large vibrations with low rate are produced at the apical end of the [basilar membrane] while large vibrations with high rate are produced at the basal end. The two can be controlled independently using cochlear implants: pulses with a range of rates can be applied via electrodes distributed along the membrane. Experiments using implant recipients showed that, at low stimulation rates, ratings of pitch on a pitch scale were proportional to the log of stimulation rate, but also decreased with distance from the round window. At higher rates, the effect of rate was weaker, but the effect of place was strong.[8]

Inner and outer hair cells

The presence of two types of hair cells, the inner and outer hair cells, in the organ of Corti was appreciated nearly a 100 years ago but the function of the two has only become clear in the last 20 years. The first clue that they might play different roles in hearing came about 40 years ago as the result of a painstaking anatomical investigation which revealed that most of the nerve

fibers that carry information to the brain contact only the inner hair cells. This meant that most the information about the acoustic world reached the brain via the inner hair cells. What then was the role of outer hair cells which are over three times more numerous? The mystery was compounded by the discovery that neural fibers originating from neurons deep in the brain, which send information back to the hair cells, only touch outer hair cells. It was later determined that outer hair cell stereocilia are firmly embedded in the overlying tectorial membrane while inner hair cell sterocilia make only a tenuous connection. The outer hair cells are located near the center of the basilar membrane where vibrations will be greatest while the basilar membrane is anchored under the inner hair cells (see Figure 5). These observations suggest that the movement of stereocilia and the resulting modulation of their ionic currents is likely to be greater for outer hair cells than for inner hair cells. Several studies that had examined the inner ears of deaf people shortly after they died demonstrated that outer hair cells were required for hearing. It was clear that the inner hair cells served to transmit information to the brain but the role of the outer hair cells remained a mystery. The mechanical vibrations of the organ of Corti had been analyzed by engineers since the 1940s. Their analysis was able to explain the frequency selectivity originally measured by von Bekesy in cochlea obtained from cadaver ears. It was known at the time that the measured frequency selectivity and the frequency selectivity computed from the engineering analysis did not approach the frequency selectivity of the human hearing or the frequency selectivity that could be measured from individual nerve fibers. Shortly after WW2 an American astrophysicist who had worked on radar during the war suggested that the frequency selectivity of the cochlea could be enhanced if a source of mechanical energy were present in the cochlea. His suggestion was largely ignored until several engineering groups in the late 70s rediscovered the potential benefits of this hypothetical energy source. They were forced to consider the possible existence of this "cochlear amplifier" when improved measures from living (as opposed to dead) ears revealed that the mechanical frequency selectivity in the living ear began to approach that of human hearing. The concept that a source of mechanical energy exists in the cochlea appeared validated when in the late 70s it was discovered that sound is produced by the inner ear. These sounds can be measured by placing a sensitive microphone in the ear canal. They were called otoacoustic emissions and they are now routinely measured in the clinic to assess hearing. Their discovery was amazing for sensory physiology because it was equivalent to finding that light comes out of the eye (which has never been observed). Within five years it was discovered that the outer hair cell could be made to elongate and shorten by electrical stimulation. The function of the outer hair cell in hearing is now perceived as that of a cochlear amplifier that refines the sensitivity and frequency selectivity of the mechanical vibrations of the cochlea.

Hair cell
From Wikipedia, the free encyclopedia

For hair cells on the external skin, see Hair follicle. For algal 'hair cells', see Trichocyte (disambiguation). See also: Stereocilia (inner ear)

Neuron: PswiandfSW

Section through the spiral organ of Corti. Magnified. ("Outer hair cells" labeled near top; "inner hair cells" labeled near center).

Location

Cochlea

Function

Amplify sound waves and transduce auditory information to the Brain Stem

Morphology

Unique (see text)

Presynaptic connections

None

Postsynaptic connections

Via auditory nerve tovestibulocochlear nerve toinferior colliculus

Gray's

subject #232 1057

NeuroLex ID

nifext_61

Hair cells are the sensory receptors of both the auditory system and the vestibular system in all vertebrates. In mammals, the auditory hair cells are located within the organ of Corti on a thin basilar membrane in the cochlea of the inner ear. They derive their name from the tufts of stereocilia that protrude from the apical surface of the cell, a structure known as the hair bundle, into the scala media, a fluid-filled tube within the cochlea. Mammalian cochlear hair cells come in two anatomically and functionally distinct types:

the outer and inner hair cells. Damage to these hair cells results in decreased hearing sensitivity, i.e. sensorineural hearing loss.
Contents
[hide]

1 Hair bundles as sound detectors and amplifiers 2 Inner hair cells from sound to nerve signal 3 Outer hair cells acoustical pre-amplifiers 4 Neural connection 5 Regrowth 6 Additional images 7 Notes 8 References 9 External links

[edit]Hair

bundles as sound detectors and amplifiers

Research of the past decades has shown that outer hair cells do not send neural signals to the brain, but that they mechanically amplify low-level sound that enters the cochlea. The amplification may be powered by movement of their hair bundles, or by an electrically driven motility of their cell bodies. The inner hair cells transform the sound vibrations in the fluids of the cochlea into electrical signals that are then relayed via the auditory nerve to the auditory brainstem and to the auditory cortex. Results in recent years further indicate that mammals apparently have conserved an evolutionarily earlier type of hair-cell motility. This so-called hair-bundle motility amplifies sound in all non-mammalian land vertebrates. It is affected by the closing mechanism of the mechanical sensory ion channels at the tips of the hair bundles. Thus, the same hair-bundle mechanism that detects sound vibrations also actively "vibrates back" and thereby mechanically amplifies weak incoming sound.

[edit]Inner

hair cells from sound to nerve signal

See also: Stereocilia (inner ear)

Section through the organ of corti, showing inner and outer hair cells

The deflection of the hair-cell stereocilia opens mechanically gated ion channels that allow any small, positively charged ions (primarilypotassium and calcium) to enter the cell.[1] Unlike many other electrically active cells, the hair cell itself does not fire an action potential. Instead, the influx of positive ions from the endolymph in Scala media depolarizes the cell, resulting in a receptor potential. This receptor potential opens voltage gated calcium channels; calcium ions then enter the cell and trigger the release of neurotransmitters at the basalend of the cell. The neurotransmitters diffuse across the narrow space between the hair cell and a nerve terminal, where they then bind toreceptors and thus trigger action potentials in the nerve. In this way, the mechanical sound signal is converted into an electrical nerve signal. The repolarization in the hair cell is done in a special manner. The Perilymph in Scala tympani has a very low concentration of positive ions. The electrochemical gradient makes the positive ions flow through channels to the Perilymph. Hair cells chronically leak Ca2+. This leakage causes a tonic release of neurotransmitter to the synapses. It is thought that this tonic release is what allows the hair cells to respond so quickly in response to mechanical stimuli. The quickness of the hair cell response may also be due to that fact that it can increase the amount of neurotransmitter release in response to a change as little as 100 V in membrane potential.[2]

[edit]Outer

hair cells acoustical pre-amplifiers

In mammalian outer hair cells, the receptor potential triggers active vibrations of the cell body. This mechanical response to electrical signals is termed somatic electromotility[3]and drives oscillations in the cells length, which occur at the frequency of the incoming sound and provide mechanical feedback amplification. A movie clip showing an isolated outer hair cell moving in response to electrical stimulation can be seen here. Outer hair cells have evolved only in mammals. While hearing sensitivity of mammals is similar to that of other classes of vertebrates, without functioning outer hair cells, the sensitivity decreases by approximately 50 dB. Outer hair cells extend the hearing range to about 200 kHz in some marine mammals.[4] They have also improved frequency selectivity (frequency discrimination), which is of particular benefit for humans, because it enabled sophisticated speech and music. The effect of this system is to non-linearly amplify quiet sounds more than large ones, so that a wide range of sound pressures can be reduced to a much smaller range of hair displacements.[5] This property of amplification is called the cochlear amplifier. The molecular biology of hair cells has seen considerable progress in recent years, with the identification of the motor protein (prestin) that underlies somatic electromotility in the outer hair cells. Santos-Sacchi et al. have shown that prestin's function is dependent on chloride channel signalling and that it is compromised by the common marine pesticidetributyltin (TBT). Because this class of pollutant bioconcentrates up the food chain, the effect is pronounced in top marine predators such as orcas and toothed whales.[6]

[edit]Neural

connection

Neurons of the auditory or vestibulocochlear nerve (the VIIIth cranial nerve) innervate cochlear and vestibular hair cells.[7] The neurotransmitter released by hair cells to stimulate the dendrites of afferent neurons is thought

to be glutamate. At the presynaptic juncture, there is a distinct presynaptic dense body or ribbon. This dense body is surrounded by synaptic vesicles and is thought to aid in the fast release of neurotransmitter. Nerve fiber innervation is much denser for inner hair cells than for outer hair cells. A single inner hair cell is innervated by numerous nerve fibers, whereas a single nerve fiber innervates many outer hair cells. Inner hair cell nerve fibers are also very heavily myelinated, which is in contrast to the unmyelinated outer hair cell nerve fibers. The region of the basilar membrane supplying the inputs to a particular afferent nerve fibre can be considered to be its receptive field. Efferent projections from the brain to the cochlea also play a role in the perception of sound. Efferent synapses occur on outer hair cells and on afferent (towards the brain) dendrites under inner hair cells. The presynaptic terminal bouton is filled with vesicles containing acetylcholine and a neuropeptide called Calcitonin generelated peptide (CGRP). The effects of these compounds varies, in some hair cells the acetylcholine hyperpolarized the cell, which reduces the sensitivity of the cochlea locally.

[edit]Regrowth
Research on the regrowth of cochlea cells may lead to medical treatments that restore hearing. Unlike fish, birds, and reptiles, post-birth humans and other mammals are normally unable to regrow the cells of the inner ear that convert sound into neural signals when those cells are damaged by age or disease.[8] There is some contradictory information regarding the possibility of hair cell regeneration in mature mammals. [9][10][11] Researchers are making progress toward gene and stem-cell therapies that may allow the damaged cells to be regenerated.[12] Researchers have identified a mammalian gene that normally acts as a molecular switch to block the regrowth of cochlear hair cells in adults.[13] The Rb1 gene encodes the retinoblastoma protein that performs several physiological functions.[14] Not only do hair cells in a culture dish regenerate when the Rb1 gene is deleted, but mice bred to be missing the gene grow more hair cells than control mice that have the gene. The cell cycle inhibitor p27kip1 has also been shown to allow regrowth of cochlear hair cells in mice following genetic deletion or knock down with siRNA targeting p27. [15][16][17]