Neuroscience · Unit 3: Sensory systems

Hearing and Balance

How does a bundle of stiff hairs turn a vibration far smaller than a cell into a current, and how does the brain use that current to tell pitch, place and head motion apart? This lesson follows the hair cell from force to transmitter, the cochlea as a frequency map with an amplifier, the brainstem circuits that compare the two ears, and the canals and otoliths that steady the eyes. Afterwards you can place a frequency on the cochlea, compute an interaural time difference, and trace the horizontal vestibulo-ocular reflex.

Watch first Pitch Becomes a Place Along the Cochlea · 2:42

One kind of cell, the hair cell, tells you that a violin is playing an A, that the violin is to your left, and that your head has just turned toward it.

The inner ear has two parts that share this cell. The cochlea, a coiled tube, analyses sound. The vestibular organs, three semicircular canals and two otolith organs, sense head motion and gravity. In both, a hair cell turns a tiny movement into a graded voltage; what differs is the mechanics around the cell and the circuits that read it. Sensory coding covers transduction and receptive fields in general.

The hair bundle: force to current

On top of each hair cell sits a hair bundle, rows of stiff stereocilia graded in height like a staircase. Many vestibular hair cells also have a true cilium, the kinocilium, beside the tallest row; mammalian cochlear hair cells lose it as they mature. Fine tip links run from the tip of each stereocilium to its taller neighbour. Each link is made of cadherin 23 and protocadherin 15, whose ends overlap in a handshake (Sotomayor and colleagues, 2012, crystal structures).

Push the bundle toward its tallest stereocilia and the tip links tighten and pull open mechanically gated cation channels. Calcium imaging in neonatal rat cochlear hair cells implies that the working channels sit at the lower end of each link (Beurg and colleagues, 2009). Push the other way and the links slacken, the channels that were open at rest close, and the cell hyperpolarizes. The gating machinery belongs to ion channels as receptors; in short, mutating a protein called TMC1 in mouse hair cells changed how ions pass, making TMC1 part of the pore (Pan and colleagues, 2018), though the full native complex is not solved.

Hudspeth and Corey (1977) measured this relation in hair cells of the bullfrog sacculus in vitro, recording intracellularly while moving single bundles. Deflection toward the kinocilium gave the depolarizing response. Voltages were graded, up to about 15 mV, with a peak slope near 20 mV per micrometre. Those numbers belong to that frog preparation, not to the human cochlea.

What carries the current? The top of the hair cell faces endolymph, a fluid rich in K+ that, in the cochlea, is held positive (by roughly +80 mV in mammals) by the endocochlear potential (vestibular endolymph is only slightly positive); making it is a transport problem (membrane transport). The driving force on an ion is the membrane potential minus that ion’s equilibrium potential (the resting membrane). In round illustrative numbers, suppose the cell sits at −50 mV and the endolymph at +80 mV, with K+ about equally concentrated on both sides of the top membrane. Equal concentrations mean K+ would be at equilibrium only with no voltage across that membrane, so the whole 130 mV pushes K+ inward. Opening channels lets K+ in, and the cell depolarizes, the reverse of most neurons, where K+ leaves.

The depolarization opens voltage-gated Ca2+ channels at the base. Mouse inner hair cells lacking the L-type channel CaV1.3 showed only marginal depolarization-evoked exocytosis (Brandt, Striessnig and Moser, 2003), so Ca2+ entry drives release, as at other synapses (synaptic transmission). The release site is a ribbon synapse. Mature mammalian cochlear hair cells, once lost, are not replaced (injury and regeneration).

The cochlea as a frequency map, and its amplifier

Cochlear hair cells sit on the basilar membrane, which runs the length of the coil. Near the base, where sound enters, the membrane is narrow and stiff; toward the apex it is wider and more compliant. Sound sets up a travelling wave that moves from base to apex, grows until it reaches the place whose stiffness suits its frequency, peaks, and dies away. High frequencies peak near the base, low frequencies near the apex. This map of frequency onto position is tonotopy, and it is kept at every relay up to cortex. Georg von Békésy measured these waves, many in human cadaver cochleas, and received the 1961 Nobel Prize. His peaks were far broader than a living ear’s tuning.

The difference is an amplifier. One row of inner hair cells supplies most of the auditory nerve’s afferent fibres. Three rows of outer hair cells receive few afferents but change length when their voltage changes, electromotility, reported in isolated guinea-pig outer hair cells by Brownell and colleagues (1985). The motor is the membrane protein prestin, driven by voltage, not by ATP. On each cycle of a sound the outer hair cells push on the membrane in step, adding energy at the peak, which sharpens tuning and raises sensitivity.

Greenwood’s function (1990) gives the frequency that peaks at each place in the human cochlea:

f = 165.4 × (10^(2.1x) − 0.88), with f in Hz and x the fraction of length measured from the apex

Worked problem: placing two tones. Where do 1,000 Hz and 4,000 Hz peak? Assume a 35 mm cochlea.

Step 1: rearrange. x = log10(f / 165.4 + 0.88) / 2.1.

Step 2: 1,000 Hz. 1000 / 165.4 = 6.046; plus 0.88 is 6.926; log10 is 0.840; divided by 2.1, x = 0.400. That is 0.400 x 35 mm = 14.0 mm from the apex, 21.0 mm from the base.

Step 3: 4,000 Hz. 4000 / 165.4 = 24.18; plus 0.88 is 25.06; log10 is 1.399; divided by 2.1, x = 0.666. That is 23.3 mm from the apex, 11.7 mm from the base.

Step 4: compare. Two octaves span 23.3 − 14.0 = 9.3 mm, and the higher tone sits nearer the base.

Placing a tone on the cochlea⚙ original · interactive

In this sketch the sliders are logarithmic in frequency, about 20 Hz to 20 kHz, the span of the Greenwood function as used here.

A

B

Higher tone
Distance apart on the membrane
Frequency ratio
One octave up from A, from B (mm)

In this sketch: the human Greenwood map, a 35 mm cochlea, peak place only; envelopes are not to scale. The rule to keep: x is measured from the apex, so the distance from the base is 35 mm minus the distance from the apex, and the higher tone peaks nearer the base.

Two ears, two cues

The auditory nerve ends in the cochlear nucleus on the same side (ipsilateral; the other side is contralateral). Above that, the pathway is bilateral. Cochlear-nucleus neurons project to the superior olivary complex on both sides; fibres ascend to the inferior colliculus in the midbrain, which supplies most of the input to the medial geniculate nucleus of the thalamus, which relays to auditory cortex in the temporal lobe (the map of the nervous system places these levels). So deafness in one ear points to the ear, the auditory nerve or the cochlear nucleus: a lesion higher up leaves each ear represented on both sides.

The two sides meet to locate sounds. An interaural time difference (ITD) is the difference in arrival time between the ears. An interaural level difference (ILD) is the difference in loudness, made because the head casts a sound shadow.

Worked problem: how large is an ITD? Treat the ears as two points 0.20 m apart, take sound speed as 343 m/s, and put a distant source at angle theta from straight ahead. The extra path to the far ear is d x sin(theta), so

ITD = d x sin(theta) / c

At 30 degrees: 0.20 m x 0.5 / 343 m/s = 0.000292 s, or 292 microseconds.

At 90 degrees: 0.20 m x 1.0 / 343 m/s = 583 microseconds.

The model ignores the path around the head, so it underestimates real ITDs; the point is the scale.

Neurons in the medial superior olive (MSO) are excited by both cochlear nuclei and fire most when the two inputs arrive together. They handle ITDs, mainly at low frequencies, where spikes can lock to the phase of the wave, firing at the same point in each cycle. Jeffress (1948) proposed that axons of graded length act as delay lines, so each coincidence detector is tuned to one ITD. Bird brainstem circuits, such as the barn owl’s, are commonly cited as fitting that scheme; in the guinea pig, McAlpine, Jiang and Palmer (2001) recorded inferior-colliculus neurons and argued for a population code compared across the two hemispheres.

Neurons in the lateral superior olive (LSO) are excited by the ear on their own side and inhibited, through a relay in the trapezoid body, by the other ear, so their rate reports which ear is louder. They handle ILDs, mainly at high frequencies, where the head shadow is large. Time at low frequencies and level at high frequencies is a tendency, not a wall.

Neither cue tells above from below. The folds of the pinna filter sound differently by elevation, and the brain learns those spectral cues: when Hofman and colleagues (1998) reshaped adults’ pinnae with moulds, elevation judgments were poor at first and then progressively recovered with the moulds in place.

Canals, otoliths and the VOR

Vestibular hair cells use the same transduction with different mechanics. Each semicircular canal is a fluid-filled ring whose swelling, the ampulla, holds hair bundles in a gelatinous flap, the cupula. When the head rotates, endolymph lags by inertia, bends the cupula and deflects the bundles, so canals report rotation. Canals on opposite sides pair in one plane, and a turn excites one partner while inhibiting the other.

The otolith organs sense linear acceleration and gravity. In the utricle, roughly horizontal when you stand, and the saccule, roughly vertical, the bundles are capped by a membrane loaded with calcium carbonate crystals. Tilting or accelerating the head shears that heavier membrane across the hair cells, and the two can give the same shear, so otolith afferents alone are ambiguous. In rhesus monkeys, Angelaki and colleagues (1999) found that after canal inactivation, eye responses to translation followed the ambiguous otolith signal, supporting the view that the brain combines canal and otolith signals to tell tilt from translation.

The canals’ main job is the vestibulo-ocular reflex (VOR), which keeps the eyes still in the world while the head moves. For a head turn to the left:

  1. The left horizontal canal is excited; the right is inhibited.
  2. The left vestibular nucleus excites the right abducens nucleus, whose motor neurons drive the right lateral rectus and turn the right eye rightward.
  3. Abducens interneurons cross and run up the medial longitudinal fasciculus (MLF) to the left oculomotor nucleus, which drives the left medial rectus and turns the left eye rightward.

Both eyes move right as the head turns left. The reflex’s gain is eye velocity divided by head velocity. In a made-up case, a head turning at 100 degrees per second with eyes counter-rotating at 80 degrees per second gives a gain of 0.80, and the image slips across the retina at 20 degrees per second. The cerebellum corrects a wrong gain. Damage to one labyrinth (the vestibular organs of one inner ear) unbalances the pair: the healthy side’s resting firing is no longer matched, and the brain reads the imbalance as rotation, one mechanism of vertigo.

Design problem

Mice lacking prestin lose sensitivity and sharp cochlear tuning. A reviewer says this does not show that outer-hair-cell electromotility is the cochlear amplifier. Why is the reviewer right, and what experiment answers the objection?

One way to do it

Deleting a protein removes everything it does. Knockout outer hair cells had reduced stiffness, and a floppier, shorter or dying cell would also weaken amplification. So the knockout shows prestin is needed, not that its motor action is.

Remove the motor and keep the rest. Dallos and colleagues (2008) made knock-in mice whose prestin carried two substitutions, V499G and Y501H, leaving little electromotility, and checked that outer-hair-cell mechanics and mechanoelectric transduction were preserved. Those mice still lost cochlear amplification, supporting a requirement for prestin-based motility.

Controls to ask for: outer-hair-cell transduction currents; counts of surviving hair cells at the ages tested; thresholds across frequencies, not one tone. Limits: this is the mouse, and the result does not exclude an additional active process in the hair bundle.

How we measure it

Intracellular recording with controlled bundle deflection

An electrode inside a hair cell records its voltage while a probe moves the hair bundle by a known distance and direction. Plotting voltage against displacement gives the cell's input-output curve and its direction sensitivity.

Heterologous expression with nonlinear-capacitance measurement

A candidate gene is expressed in a cell that normally lacks it, here prestin in cultured kidney cells, and the cell is tested for voltage-driven shape change and voltage-dependent charge movement. It shows what the protein can do alone, not whether the ear needs it.

Knock-in mutation with mechanical and transduction controls

An engineered point mutation impairs one function of a protein while the experimenter checks that other properties, such as stiffness and transduction currents, are preserved. It is the step that turns a knockout's correlation into a test of necessity.

Eye-movement recording with canal inactivation

Eye movements are measured in a monkey on a motion platform during tilts and translations, before and after the semicircular canals are inactivated. Comparing the two shows how much the brain relies on canal signals to interpret the otoliths.

Finish line

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Tip-link cadherins — the protocadherin 15 and cadherin 23 handshake
Tip-link cadherins — the protocadherin 15 and cadherin 23 handshake ● LIVE · RCSB PDB 4APX
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Loading live structure 4APX from RCSB PDB…

The tips of the two cadherins overlap in an antiparallel complex. This joint sits in the middle of the tip link that pulls on the transduction channel when the bundle moves.

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Worm TMC-1 complex — a structural model of the transduction channel
Worm TMC-1 complex — a structural model of the transduction channel ● LIVE · RCSB PDB 7USW
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Loading live structure 7USW from RCSB PDB…

Two copies each of TMC-1, CALM-1 and TMIE. It is a worm structure, so use it as a model for comparison with mouse functional data on TMC1, not as the mammalian channel itself.

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A. James Hudspeth and David Corey

A. James Hudspeth and David Corey

Recorded intracellularly from hair cells of the bullfrog sacculus in vitro while moving single hair bundles, and showed that the receptor potential is graded and depends on the direction of deflection.

Hair cells were known to sit under every sensory surface of the inner ear, but how a mechanical push became an electrical signal in a single cell was only beginning to be measured. Corey was a graduate student at Caltech, and Hudspeth advised his doctoral work. They used the sacculus of the bullfrog, Rana catesbeiana, an organ whose hair cells are large and easy to reach in a dish. With a fine probe they pushed individual hair bundles by known distances while recording the cell's voltage with an intracellular electrode. Deflection toward the kinocilium, the side with the tallest stereocilia, depolarized the cell; deflection the other way hyperpolarized it. Responses grew smoothly with displacement, up to about 15 mV, and at its steepest the slope was about 20 mV per micrometre. They published the work in PNAS in 1977. A direct input-output curve for one hair cell gave later workers a quantity to explain, and a test bed for the search for the transduction channel and the tip link.

✓ verbatim Hudspeth & Corey, Proc. Natl. Acad. Sci. USA 74:2407–2411 (1977); CaltechTHESIS record of Corey's doctoral dissertation (1980).
Georg von Békésy

Georg von Békésy

Measured the travelling wave of the basilar membrane and showed that each frequency produces its largest motion at a different place along the cochlea, for which he received the 1961 Nobel Prize in Physiology or Medicine.

Von Békésy came to the ear from physics and engineering rather than medicine. According to a University of Hawaii finding aid for his papers, he worked for the Hungarian Post Office on long-distance telephone transmission, where he studied the ear too, and his research turned to how the ear itself analyses sound. He opened cochleas, many of them from human cadavers, and built enlarged models of the cochlear duct, then watched how the basilar membrane moved when the fluid was driven at different frequencies. Each tone set up a wave that travelled from the base toward the apex, grew to a peak and then died away, and the place of the peak moved with frequency. In dead cochleas the peaks were broad, so his measurements could not show the sharp tuning that living ears have. The Nobel Assembly awarded him the 1961 prize for his discoveries about how the cochlea is stimulated. His wave gave the frequency map a physical mechanism, and the gap between his broad peaks and sharp living tuning pointed later workers toward an active amplifier.

✓ verbatim NobelPrize.org, The Nobel Prize in Physiology or Medicine 1961 (summary and Nobel lecture); University of Hawaii finding aid for the Georg von Békésy papers.
Peter Dallos

Peter Dallos

With colleagues, identified prestin as the motor protein of outer hair cells and tested, with a knock-in mouse, whether prestin-driven motility is needed for cochlear amplification.

In 1985 Brownell, Bader, Bertrand and de Ribaupierre reported that isolated outer hair cells from the guinea pig change length when stimulated electrically. That electromotility was a candidate for the amplifier that von Békésy's dead cochleas lacked, but the molecule behind it was unknown. In 2000 Zheng, Dallos and colleagues identified a protein enriched in outer hair cells, named it prestin, and expressed it in cultured human kidney cells. Those cells now changed shape when their voltage changed and showed the nonlinear capacitance that is the electrical signature of outer-hair-cell motility. Showing that a motor exists is different from showing that hearing needs it. Removing prestin altered outer hair cells in other ways, including their stiffness. So in 2008 the Dallos laboratory reported mice carrying a prestin with two substitutions, V499G and Y501H, that left little motility while hair-cell mechanics and transduction were preserved, and those mice lost cochlear amplification. The knock-in turned a correlation into a test of necessity in the mouse.

✓ verbatim Zheng et al., Nature 405:149–155 (2000); Dallos et al., Neuron 58:333–339 (2008); Brownell et al., Science 227:194–196 (1985).
Lloyd Jeffress

Lloyd Jeffress

Proposed in 1948 that the brain could compute interaural time differences with delay lines feeding coincidence-detecting neurons, so that position along a nucleus would encode azimuth.

A sound straight ahead reaches both ears together; a sound off to one side reaches the nearer ear a fraction of a millisecond sooner. Jeffress asked what kind of neural circuit could read such a small difference. In a short paper in the Journal of Comparative and Physiological Psychology in 1948 he proposed one. Axons from the two ears run in opposite directions along a row of neurons, so that each neuron sits at a different extra travel time from each side. A neuron fires best only when inputs from both ears arrive together, making it a coincidence detector, so the neuron that fires most marks the delay that the head imposed. The scheme was a model, with no recordings behind it. Work in birds later found brainstem circuits that fit it well. In the guinea pig, McAlpine, Jiang and Palmer recorded inferior-colliculus neurons in 2001 and argued instead for a population code that compares activity in the two hemispheres. Jeffress's model gave the field a precise hypothesis to test, species by species.

✓ verbatim Jeffress, J. Comp. Physiol. Psychol. 41:35–39 (1948); McAlpine, Jiang & Palmer, Nat. Neurosci. 4:396–401 (2001).
Test yourself
Question 1 of 8 Score 0 / 0

A hair bundle is pushed toward its tallest stereocilia. What happens first?
Sources & Integrity

Every structure, slide, simulation, and clip on this page is listed below with the source it came from. None of the 3D structures is drawn by hand or by AI: each one loads by accession ID from RCSB PDB or PubChem. This panel is generated from the lesson's own data file, so what it lists is what the page loads.

Molecular structures live data

  • Tip-link cadherins — the protocadherin 15 and cadherin 23 handshake — RCSB PDB 4APX · coordinates CC0 · Mouse cadherin-23 and protocadherin-15 N-terminal fragments, X-ray crystal structure (Sotomayor, Weihofen, Gaudet and Corey, Nature, 2012)
  • Worm TMC-1 complex — a structural model of the transduction channel — RCSB PDB 7USW · coordinates CC0 · Native C. elegans TMC-1 complex, cryo-EM (Jeong and colleagues, Nature, 2022); one of three deposited states

Simulations

  • Where a tone peaks · Original interactive — Biochemistrypedia (Deppmann Lab).

Scientist profiles & quotes

  • A. James Hudspeth and David Corey — Hudspeth & Corey, Proc. Natl. Acad. Sci. USA 74:2407–2411 (1977); CaltechTHESIS record of Corey's doctoral dissertation (1980).
  • Georg von Békésy — NobelPrize.org, The Nobel Prize in Physiology or Medicine 1961 (summary and Nobel lecture); University of Hawaii finding aid for the Georg von Békésy papers.
  • Peter Dallos — Zheng et al., Nature 405:149–155 (2000); Dallos et al., Neuron 58:333–339 (2008); Brownell et al., Science 227:194–196 (1985).
  • Lloyd Jeffress — Jeffress, J. Comp. Physiol. Psychol. 41:35–39 (1948); McAlpine, Jiang & Palmer, Nat. Neurosci. 4:396–401 (2001).

Quotes are verbatim from the cited source. Profile text is original to this site and was checked against the sources cited.

Animated explainer

Pitch Becomes a Place Along the Cochlea · narration: an AI narrator voice (Gemini, Charon) reading narration written from this lesson's text · animation: AI-generated in code (Manim) by Claude, a schematic with no drawn molecular structures, plots computed from their equations · captions from the narration script.

Images & figures

This lesson carries no raster figures. Every structure is rendered live from RCSB PDB or PubChem, and every plot is drawn from its equation in the browser.

integrity Machines check the mechanics. The build confirms that every local file exists, that every question's answer key points at a real choice, and that any AI-generated scientific figure names the person who checked it; a weekly job re-resolves every accession ID against its database. Questions are original; MCAT-style items are written for this site and are not real AAMC questions. Banned sources (the Tymoczko textbook, publisher decks, copyrighted figures) are not used.

Like I'm five

Deep in your ear are cells with tiny hairs on top. When sound or a head movement wiggles the hairs one way, the cell gets excited; when they wiggle the other way, it calms down. In the snail-shaped part of the ear, different spots wiggle for high and low sounds, so the brain knows the pitch from which spot is busy. Other hair cells feel your head turning and tilting and tell your eyes to move the other way so the world stays still.
High school

Hair cells are the sensors of the inner ear. Bending their bundle of stiff stereocilia toward the tallest ones pulls on fine links that open channels, letting positively charged potassium ions flow in from the fluid above, so the cell depolarizes and releases transmitter onto the auditory nerve. In the cochlea a membrane runs along a coiled tube; its stiff end vibrates most to high pitches and its floppy end to low pitches, giving a map of frequency. Outer hair cells push back on the membrane to amplify faint sounds. The brain locates sounds by comparing the two ears: which ear the sound reached first, and which heard it louder. In the vestibular system, canals sense head rotation and the otolith organs sense tilt and straight-line movement, and the vestibulo-ocular reflex moves the eyes opposite to the head.
College

Deflecting a hair bundle toward its tallest stereocilia tensions tip links, made of cadherin 23 and protocadherin 15, and opens mechanically gated cation channels near the lower ends of the links. The apical membrane faces K+-rich endolymph, held positive by the endocochlear potential, so the inward current is carried mainly by K+ and the cell depolarizes in a graded way; Ca2+ entry through L-type channels at the base drives release at ribbon synapses onto auditory-nerve fibres, most of which contact inner hair cells. The basilar membrane's stiffness gradient makes a travelling wave peak near the base for high frequencies and near the apex for low ones, and prestin-driven electromotility of outer hair cells amplifies and sharpens that peak. Above the cochlear nucleus the pathway is bilateral: the MSO compares arrival times for low frequencies, the LSO compares levels for high frequencies, and pinna filtering supplies elevation cues. Canals sense angular acceleration through cupula deflection, otoliths sense gravito-inertial acceleration, and the horizontal VOR uses a three-neuron arc to rotate the eyes opposite to the head.
Graduate

In the bullfrog sacculus, Hudspeth and Corey measured graded receptor potentials up to about 15 mV with a peak sensitivity near 20 mV per micrometre; calcium imaging in neonatal rat cochlear hair cells placed functional channels at the lower ends of tip links, and cysteine-substitution experiments in mouse hair cells made TMC1 a pore component, while the worm TMC-1 complex (with CALM-1 and TMIE) supplies a structural model whose transfer to mammals is still being tested. How force reaches the gate, and what other proteins complete the native complex, is open.

Cochlear amplification in the mouse requires prestin-based electromotility, by the knock-in test, but an active process in the hair bundle itself has not been excluded, and how the two share the work across frequencies is debated. In the binaural system, the delay-line model fits bird data, while guinea-pig inferior-colliculus recordings support a population code across the two hemispheres. In the vestibular system, otolith afferents are ambiguous between tilt and translation, and rhesus-monkey experiments with canal inactivation show that canal signals contribute to resolving that ambiguity, at least above about 0.1 Hz.
A hearing motor in a kidney cell

To test whether a single protein could explain outer-hair-cell electromotility, Zheng and colleagues took prestin out of the ear altogether. They expressed it in cultured human kidney cells, which have no business changing length. The transfected cells changed shape when their membrane voltage changed, and they also showed nonlinear capacitance, the voltage-dependent charge movement measured in outer hair cells. The experiment showed that prestin is enough to produce the motor behaviour in another cell. It could not show that the cochlea needs that motor; that took the knock-in mice eight years later.

— Zheng, Shen, He, Long, Madison & Dallos, Nature 405:149–155 (2000).
New ears for adults

The folds of the outer ear filter sound differently depending on where it comes from above or below, and the brain uses those spectral cues to judge elevation. Hofman and colleagues fitted adult volunteers with moulds that changed the shape of their pinnae. At first the listeners localized sounds in elevation poorly. With time their accuracy progressively recovered with the moulds still in place. The study shows that the adult human brain keeps calibrating the spectral cues it relies on, though behaviour alone could not say where in the brain that relearning happened.

— Hofman, Van Riswick & Van Opstal, Nature Neuroscience (1998), doi:10.1038/1633.
Tilt or travel?

An otolith organ cannot tell a head tilted sideways from a head accelerating sideways, because both shear the otolithic membrane in the same way. Angelaki and colleagues tested how the brain copes in rhesus monkeys, comparing eye movements during roll tilt, translation and combinations designed to give the otoliths the same stimulus. After the semicircular canals were inactivated, the translational eye responses followed the resultant acceleration rather than the real translation. The authors bounded the conclusion to the frequencies above about 0.1 Hz where the reflex matters for gaze.

— Angelaki, McHenry, Dickman, Newlands & Hess, Journal of Neuroscience 19:316 (1999), doi:10.1523/JNEUROSCI.19-01-00316.1999.

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