Hair cell

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Hair cells or hair sensory cells are a type of secondary sensory cells (receptors) in the nervous system of vertebrates that convert mechanical stimuli into nerve activity. They carry apical stereocilia and thus belong to the class of mechanoreceptors . Hair cells can be excited by sound, water currents, rotational or linear acceleration, depending on their type. The hair cells of the mammalian inner ear have been studied best .


Hair cells consist of the cell body and the eponymous hair-like structures that serve to absorb the stimulus. This hair bundle sits on the top of the cell and consists of a cilia (kinozilia) and several stereovilli . In humans, the cilia of the cochlea's hair cells, in contrast to those of the equilibrium , are regressed after birth. The individual stereovilli are connected to one another at the tips, these connections are called "tip links". At the lower end of the cell, opposite the hair bundle, there is a region in which the excitation of the hair cell leads to the release of messenger substances, the neurotransmitters . Here, hair cells form synapses with interneurons that carry the information in the form of action potentials to the central nervous system (CNS) .


Stimulus uptake - transduction

Schematic representation of the function of a hair cell. Left: inhibition, middle: without irritation, right: arousal.
Schematic representation of the channel relationships of a hair cell when deflected

The structure of the inner hair cells, which is decisive for the absorption of stimuli, forms the hair bundle. The individual stereovilli are connected at the tips by the tip links. At the lower end of these connections (on the shorter stereovillus) is the ion channel , the so-called transduction channel , which is opened or closed by the tip link depending on the voltage. However, the molecule that forms the transduction channel has not yet been identified. The opening of the channels leads to an influx of positive potassium ions, which depolarize the cell . Without a deflecting force acting on the hair bundle, the channels are only partially open - so the cell is moderately excited at rest. When the stereovilli are deflected in the direction of the cilia, the channels are opened and the influx of potassium causes the hair cells to be excited. Deflections against the cilia close the channels. Movements on an axis other than that determined by the arrangement of the cilia do not lead to a change in the channel opening and thus play no role in the state of excitation of the cell.

Forwarding the excitement

In contrast to primary sensory cells, the hair sensory cells (secondary sensory cells) do not develop an action potential . This could not be generated at all with the high speed of the acoustically moving receptor. The amount of the emitted transmitter is rather determined by the level of the receptor potential .

Transduction mechanism of the hair cells in the inner ear

In the cochlea of the human inner ear there are three rows of outer and one row of inner hair cells. The sensory recording of mechanical movements in the cochlea occurs almost exclusively through the inner hair cells, while the outer hair cells v. a. efferent innervation obtained by higher-level centers of the CNS. In principle, the mechanical deflection of the (inner) hair cells in the inner ear is transduced into an electrical signal as described above through the influx of potassium ions. However, there are some specifics.

Ion distribution

The lower, basal part of the hair cell is surrounded by the lymph of Corti, which is located in the inner and outer tunnel and the nuel space of the organ of Corti and which is similar in its composition to the perilymph - the fluid that the scala vestibuli (and Scala tympani ) fills. The tip of the hair cell with the stereovilli is located in the endolymph of the scala media . The perilymph has a high concentration of sodium and a low concentration of potassium ions. In the endolymph, this ratio is reversed (many potassium ions, few sodium ions). There is a voltage difference between these two outer areas of the hair cell: the endolymph (above) is positively charged +85 mV compared to the perilymph (below). In the resting position (when the stereovilli are not deflected), the cytoplasm of the hair cell is negatively charged compared to the perilymph. In the upper part of the hair cell, which is surrounded by the endolymph fluid, there is a voltage gradient of −155 mV between the cell interior and the environment. In the lower cell area, which is surrounded by the perilymph, there is a voltage difference to the surrounding area of ​​−70 mV.


If the stereovilli of the hair cells are deflected by mechanical vibrations of the basilar membrane of the cochlea in the direction of the longest stereocilium, this causes the opening of potassium channels in the hair cells (as described above) via tip-link connections. In the upper area of ​​the hair cell (endolymph fluid) there is an influx of K ions. This influx comes about because the inside of the cell is 155 mV more negatively charged than the endolymph. This leads to positive charges flowing in in the form of K ions. The chemical equilibrium potential of potassium is 0 mV, because the intracellular concentration is the same as in the endolymph, but with the electrical potential of –155 mV it “strives” to positive the voltage difference between the cell exterior and interior. The potassium ions cause calcium channels to open inside the cell, which causes calcium to flow in. As in other neurons, this leads to depolarization and thus to the increased release of neurotransmitters to downstream neurons.


The peculiarity of transduction is that potassium is responsible for both de- and repolarization. The potassium ions that have flowed into the upper part of the hair cell in turn lead to the opening of further potassium channels in the entire cell membrane. The increased calcium present due to the depolarization leads u. a. also for opening K-channels. In the lower cell area surrounded by perilymph, however, there is a lower voltage difference to the surroundings at −45 mV than in the upper area. The potassium that has flown in at the top flows out again through potassium channels in the lower part of the cell, there

  • in the perilymph there is a very low potassium concentration compared to the inside of the cell
  • Potassium strives to produce its equilibrium potential of −80 mV

The latter means that positive charges in the form of K ions have to flow out in order to reduce the voltage difference from −45 mV to −80 mV. The outflow of potassium causes the hair cell to repolarize.

Motor function of the hair bundles

Images with a Scanning Electron Microscope of the hair bundle of two outer hair cells (for mammals ). Bundle shape: left V-type, right W-type.

Recent research has shown that the bundles of stereocilia (hair bundles) in the inner ear of terrestrial vertebrates have the function of motors ( motility ) in addition to their function as mechanoreceptors . Here the mechano-electrical converters in the ends of the stereocilia work in the opposite direction, i.e. as electro-mechanical converters. They give off energy and thus amplify the sound waves that stimulate them. According to previous hypotheses, this identity of the sensor and motor functions of the stereocilia serves to improve frequency coordination and thus the frequency resolution of the hearing organ. In non-mammals, this hypothesis is now proven and widely accepted. In mammals , where there is also the special feature of the motor function of the cell body of the outer hair cells ( cochlear amplifier ), it has not yet been clarified how hair bundle motors and cell body motors interact in detail.


  1. ^ David P. Corey (2006): What is the hair cell transduction channel? , J. Physiol. 576: 23-28.
  2. ^ Zenner H.-P .: Listen. Physiology, biochemistry, cell and neurobiology. G. Thieme Verlag, Stuttgart, 1994.
  3. Klinke, Silbernagl, 2005 edition, p. 664
  4. James O. Pickles: An Introduction to the Physiology of Hearing , Bingley, Emerald Group Publishing 2012, 430 pp. ISBN 1-78052-166-9 , pp. 135 and 137.

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