Editing Cochlea (section)

==Function==
[[File:Journey of Sound to the Brain.ogg|thumb|How sounds make their way from the source to the brain|400x400px]]
The cochlea is filled with a watery liquid, the [[endolymph]], 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 cell]]s sense the motion via their [[stereocilia (inner ear)|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 potential]]s, which travel along the auditory nerve to structures in the brainstem for further processing.

===Hearing===
{{Main|Hearing}}

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 ''vestibular duct'' (upper chamber of the cochlea). The ossicles are essential for efficient coupling of sound waves into the cochlea, since the cochlea environment is a fluid–membrane system, and it takes more pressure to move sound through fluid–membrane waves than it does through air. A pressure increase is achieved by reducing the area ratio from the tympanic membrane (drum) to the oval window (''stapes'' bone) by 20. As pressure = force/area, results in a pressure gain of about 20 times 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 fluid–membrane system.

At the base of the cochlea, each 'duct' ends in a membranous portal that faces the middle ear cavity: The [[vestibular duct]] 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 ducts up and down, the waves have a corresponding symmetric part in perilymph of the tympanic duct, which ends at the round window, bulging out when the oval window bulges in.

The perilymph in the vestibular duct and the [[endolymph]] in the cochlear duct act mechanically as a single duct, being kept apart only by the very thin [[Reissner's membrane]].
The vibrations of the endolymph in the cochlear duct 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 cell]]s further amplifying these vibrations. [[Inner hair cell]]s 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]].<ref>{{cite journal |last1=Nin |first1=Fumiaki |last2=Hibino |first2=Hiroshi |last3=Doi |first3=Katsumi |last4=Suzuki |first4=Toshihiro |last5=Hisa |first5=Yasuo |last6=Kurachi |first6=Yoshihisa |title=The endocochlear potential depends on two K + diffusion potentials and an electrical barrier in the stria vascularis of the inner ear |journal=Proceedings of the National Academy of Sciences |date=5 February 2008 |volume=105 |issue=5 |pages=1751–1756 |doi=10.1073/pnas.0711463105|doi-access=free |pmid=18218777 |pmc=2234216 }}</ref>

The hair cells in the organ of Corti are tuned to certain sound frequencies by way of their location in the cochlea, due to the degree of stiffness in the basilar membrane.<ref>{{cite journal |author = Guenter Ehret |date = Dec 1978 |title = Stiffness gradient along the basilar membrane as a way for spatial frequency analysis within the cochlea |url = http://vts.uni-ulm.de/docs/2009/6797/vts_6797_9398.pdf |journal = J Acoust Soc Am | volume = 64 |issue = 6|pages = 1723–6 |pmid = 739099 | doi=10.1121/1.382153}}</ref> This stiffness is due to, among other things, the thickness and width of the basilar membrane,<ref>{{Cite book |last=Camhi |first=Jeffrey M. |url=https://archive.org/details/neuroethologyner0000camh |title=Neuroethology : nerve cells and the natural behavior of animals |date=1984 |publisher=Sunderland, Mass. : Sinauer Associates |isbn=978-0-87893-075-3}}</ref> 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 vibrations as they travel through the fluid-filled coil.<ref>{{cite journal |vauthors=Manoussaki D, Chadwick RS, Ketten DR, Arruda J, Dimitriadis EK, O'Malley JT |year = 2008 | title = The influence of cochlear shape on low-frequency hearing |journal = Proc Natl Acad Sci U S A |volume = 105 |issue = 16| pages = 6162–6166 |doi = 10.1073/pnas.0710037105 |pmid=18413615 |pmc=2299218 |bibcode = 2008PNAS..105.6162M |doi-access = free }}</ref>  This spatial arrangement of sound reception is referred to as [[tonotopy]].

For very low frequencies (below 20&nbsp;Hz), the waves propagate along the complete route of the cochlea – differentially up vestibular duct and tympanic duct all the way to the ''helicotrema''. Frequencies this low still activate the organ of Corti to some extent but are too low to elicit the perception of a [[pitch (psychophysics)|pitch]].  Higher frequencies do not propagate to the ''helicotrema'', 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 [[earmuff]]s or [[earplug]]s.

=== Pathway to the brain ===
To transmit the sensation of sound to the brain, where it can be processed into the perception of ''hearing'', hair cells of the cochlea must convert their mechanical stimulation into the electrical signaling patterns of the nervous system. Hair cells are modified [[neuron]]s, able to generate action potentials which can be transmitted to other nerve cells. These action potential signals travel through the [[vestibulocochlear nerve]] to eventually reach the anterior [[Medulla oblongata|medulla]], where they [[synapse]] and are initially processed in the [[Cochlear nucleus|cochlear nuclei]].<ref name=":0">{{Cite book |last=Martin |first=John Harry |title=Neuroanatomy: Text and Atlas |publisher=McGraw Hill |year=2021 |isbn=978-1-259-64248-7 |edition=5th |location=New York |language=English |chapter=Chapter 8: The Auditory System}}</ref>

Some processing occurs in the cochlear nuclei themselves, but the signals must also travel to the [[superior olivary complex]] of the [[pons]] as well as the [[Inferior colliculus|inferior colliculi]] for further processing.<ref name=":0" />

===Hair cell amplification===
Not only does the cochlea "receive" sound, a healthy cochlea ''generates'' and amplifies sound when necessary.  Where the organism needs a mechanism to hear very faint sounds, the cochlea amplifies by the reverse [[Transduction (physiology)|transduction]] of the OHCs, converting electrical signals back to mechanical in a positive-feedback configuration.  The OHCs have a protein motor called [[prestin]] on their outer membranes; it generates additional movement that couples back to the fluid–membrane wave. This "active amplifier" is essential in the ear's ability to amplify weak sounds.<ref>{{Cite journal|last=Ashmore|first=Jonathan Felix|author-link=Jonathan Ashmore|year=1987|title=A fast motile response in guinea-pig outer hair cells: the cellular basis of the cochlear amplifier|journal=[[The Journal of Physiology]]|language=en|volume=388|issue=1|pages=323–347|doi=10.1113/jphysiol.1987.sp016617|issn=1469-7793|pmid=3656195 |pmc=1192551}} {{open access}}</ref><ref>{{Cite journal|last=Ashmore|first=Jonathan|s2cid=17722638|author-link=Jonathan Ashmore|date=2008|title=Cochlear Outer Hair Cell Motility|journal=[[Physiological Reviews]]|language=en|volume=88|issue=1|pages=173–210|doi=10.1152/physrev.00044.2006|issn=0031-9333|pmid= 18195086}} {{open access}}</ref>

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).

===Otoacoustic emissions===

[[Otoacoustic emission]]s 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. Otoacoustic emissions also exhibit sex dimorphisms, since females tend to display higher magnitudes of otoacoustic emissions. Males tend to experience a reduction in otoacoustic emission magnitudes as they age. Women, on the other hand, do not experience a change in otoacoustic emission magnitudes with age.<ref>Mishra, Srikanta K.1,2; Zambrano, Samantha2,3; Rodrigo, Hansapani4. Sexual Dimorphism in the Functional Development of the Cochlear Amplifier in Humans. Ear and Hearing 42(4):p 860-869, July/August 2021. | DOI: 10.1097/AUD.0000000000000976</ref>

===Role of gap junctions===
Gap-junction proteins, called [[connexin]]s, expressed in the cochlea play an important role in auditory functioning.<ref>{{Cite journal | last1 = Zhao | first1 = H. -B. | last2 = Kikuchi | first2 = T. | last3 = Ngezahayo | first3 = A. | last4 = White | first4 = T. W. | title = Gap Junctions and Cochlear Homeostasis | doi = 10.1007/s00232-005-0832-x | journal = Journal of Membrane Biology | volume = 209 | issue = 2–3 | pages = 177–186 | year = 2006 | pmid = 16773501 | pmc =1609193 }}</ref> Mutations in gap-junction genes have been found to cause syndromic and nonsyndromic deafness.<ref>{{Cite journal | last1 = Erbe | first1 = C. B. | last2 = Harris | first2 = K. C. | last3 = Runge-Samuelson | first3 = C. L. | last4 = Flanary | first4 = V. A. | last5 = Wackym | first5 = P. A. | title = Connexin 26 and Connexin 30 Mutations in Children with Nonsyndromic Hearing Loss | doi = 10.1097/00005537-200404000-00003 | journal = The Laryngoscope | volume = 114 | issue = 4 | pages = 607–611 | year = 2004 | pmid = 15064611 | s2cid = 25847431 }}</ref>  Certain connexins, including [[GJB6|connexin 30]] and [[GJB2|connexin 26]], are prevalent in the two distinct gap-junction systems found in the cochlea.  The epithelial-cell gap-junction network couples non-sensory epithelial cells, while the connective-tissue gap-junction network couples connective-tissue cells.<ref>{{cite journal |last1=Wang |first1=Bo |last2=Hu |first2=Bohua |last3=Yang |first3=Shiming |title=Cell junction proteins within the cochlea: A review of recent research |journal=Journal of Otology |date=December 2015 |volume=10 |issue=4 |pages=131–135 |doi=10.1016/j.joto.2016.01.003|pmid=29937796 |pmc=6002592 }}</ref>  Gap-junction channels recycle potassium ions back to the endolymph after [[mechanotransduction]] in [[hair cells]].<ref>{{Cite journal | doi = 10.1016/S0165-0173(99)00076-4 | last1 = Kikuchi | first1 = T. | last2 = Kimura | first2 = R. S. | last3 = Paul | first3 = D. L. | last4 = Takasaka | first4 = T. | last5 = Adams | first5 = J. C. | title = Gap junction systems in the mammalian cochlea | journal = Brain Research. Brain Research Reviews | volume = 32 | issue = 1 | pages = 163–166 | year = 2000 | pmid = 10751665| s2cid = 11292387 }}</ref>  Importantly, gap junction channels are found between cochlear supporting cells, but not auditory [[hair cells]].<ref>{{Cite journal | doi = 10.1007/BF00186783 | last1 = Kikuchi | first1 = T. | last2 = Kimura | first2 = R. S. | last3 = Paul | first3 = D. L. | last4 = Adams | first4 = J. C. | title = Gap junctions in the rat cochlea: Immunohistochemical and ultrastructural analysis | journal = Anatomy and Embryology | volume = 191 | issue = 2 | pages = 101–118 | year = 1995 | pmid = 7726389| s2cid = 24900775 }}</ref>