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810 NATURE|VOL433|24FEBRUARY2005|www.nature.com/nature
decrease in the nutrient availability, like that
broughtaboutbytheseasurfacebeingcutoff
from the deeper ocean, at least on a seasonal
basis.At the same time,the reduction in ver-
tical mixing allows the sea surface to warm.
Thus the development of a seasonally lay-
ered, or stratified, surface ocean 2.7 million
years ago, which was probably a regional
response to the large-scale climatic changes
at this time12
, allowed late summer/autumn
warming of the sea surface and provided a
moisturesourceforicegrowth.
Haug et al.8
test the interpretations of the
geochemical records with a suite of numeri-
cal computer-model experiments. The sim-
ulated ocean is `stratified' and `destratified'
to determine whether this mechanism can
account for the geochemically derived
changes in temperature. And it can. The
stratifiedmodelstateproducesmoreextreme
seasons and a larger North American ice
sheetthandoesthedestratifiedmodel.
This is an exemplary study. The individ-
ual climate indicators may not have with-
stood the uncertainties and assumptions
that limit each of them, but put together by
Haug et al. they tell a cogent story of the
originof theiceages. 
Katharina Billups is at the College of Marine
Studies, University of Delaware, 700 Pilottown
Road, Lewes, Delaware 19958, USA.
e-mail: kbillups@udel.edu
1. Zachos, J. et al. Science 292, 686­693 (2001).
2. Raymo, M. E. & Ruddiman, W. F. Nature 359, 117­122 (1992).
3. Pearson, P. N. & Palmer, M. R. Nature 406, 695­699 (2000).
4. Milankovitch, M. Serb. Akad. Beogr. Spec. Publ. 132 (1941).
5. Haug, G. H. & Tiedemann, R. Nature 393, 673­676 (1998).
6. Driscoll, N. W. & Haug, G. H. Science 282, 436­438 (1998).
7. Ravelo, A. C. et al. Nature 429, 263­267 (2004).
8. Haug, G. H. et al. Nature 433, 821­825 (2005).
9. Wefer, G., Berger, W. H., Bijma, J. & Fischer, G. in Use of Proxies
in Paleoceanography (eds Fischer, G. & Wefer G.) 1­68
(Springer, Berlin, 1999).
10.Brandiss, M. E., O'Neil, J. R., Edlund, M. B. & Stoermer, E. F.
Geochim. Cosmochim. Acta 62, 1119­1125 (1998).
11.Emiliani, C. J. Geol. 63, 538­578 (1955).
12.Haug, G. H. et al. Nature 401, 779­782 (1999).
Hearing
Aid from hair force
Corné Kros
Mammals hear with exquisite sensitivity and precision over a huge
range of frequencies; tiny amplifiers in the inner ear make this possible.
New results challenge current thinking on how these amplifiers work.
O
ur ability to hear relies on cells in the
inner ear called hair cells -- named
after the bundle of 100 or so hair-
like projections that protrudes from their
upper surfaces. Sound bends the hair bun-
dles, causing small electrical (`transducer')
currents to flow, which in turn makes the
hair cells signal the reception of sound to
the brain. In mammals, the silent majority
of the hair cells (the outer hair cells) do not
talk to the brain, instead helping the inner
hair cells -- the true sensory receptors -- to
do so with more clarity than they could
achieve by themselves. But how is this done?
For two decades scientists have sought
the answer in the extraordinary ability of the
outerhaircellstochangetheirlengthrapidly
when stimulated. Now, however, Kennedy,
Crawford and Fettiplace1
(page 880 of this
issue) and Chan and Hudspeth2
(in Nature
Neuroscience) present provocative evidence
that the main component of the elusive
`cochlear amplifier'may instead reside in the
hairbundlesof theouterhaircells.
Sound waves that reach the ear lead to
vibrationsinsidethecochlea--afluid-filled,
coiled tube forming the auditory part of the
inner ear (Fig. 1a). The sensory hair cells
reside in a thin strip of tissue, the organ of
Corti, that is wedged between two mem-
branes of the cochlea.The vibrations cause a
shearing motion between these two mem-
branes, which bends the hair bundles. Like a
rolled-up piano, one end of the organ of
Cortivibratesbestatlowfrequenciesandthe
otherathighfrequencies.Innormalears,the
vibration is boosted and sharpened for soft
sounds by what has become known as the
cochlearamplifier3
.
Twenty years ago,a remarkable discovery
by Brownell and colleagues4
seemed to show
what the cochlear amplifier is made of: they
foundthatelectricalstimulationof theouter
hair cells made them lengthen and shorten
their cell bodies. The idea is that, in vivo, the
electricity produced by bending the hair
bundles would drive this lengthening and
shortening, or electromotility, as fast as
sound could vibrate the bundles.The strate-
gic position of the outer hair cells would
locally boost the vibration of the organ of
Corti, and in this way stimulate, by fluid
coupling,thebundlesoninnerhaircells.
At a molecular level, this mechanism is
thought to rely on a motor protein called
prestin, named from the musical term for a
very fast tempo.The basolateral membranes
of the outer hair cells are packed with this
protein5
, which changes shape as fast as you
canchangethevoltageacrossthemembrane,
over a range of frequencies up to at least 100
kHz (ref. 6). But there is a snag: although
prestin is quick, it is not clear whether the
transmembrane voltage in vivo changes
much over the period of the sound wave, at
sound frequencies greater than a few kilo-
hertz. This is because the receptor potential
due to the transducer currents is severely
attenuated at higher frequencies by the
electricalimpedanceof thecell7
.
An alternative source of force that is not
voltage-dependent may thus be needed to
power the cochlear amplifier. Kennedy and
colleagues1
report large forces generated by
thehairbundlesofratouterhaircellsinvitro,
when stimulated by a flexible glass fibre.You
would expect the tip of the fibre to move less
when attached to the bundle than when it is
freelymovinginthefluid.Sotheremusthave
been disbelief in the lab when,in some cases,
the fibre moved further when coupled to the
hair bundles, implying that a force in the
bundle drags the fibre along, instead of the
otherwayround.
Thisforce--anorderofmagnitudelarger
than the force that is a necessary by-product
of opening the ion channels through which
the transducer current enters hair cells8
-- is
not there at the moment the hair bundle
is moved by the fibre, but develops within
a fraction of a millisecond. Its time course
is closely coupled to that over which the
transducer current adapts to a steady
Figure 2 Icy evidence in the Northern Hemisphere: a present-day ice-sheet on the Svalbard Islands.
DAVEG.HOUSER/CORBIS
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NATURE|VOL433|24FEBRUARY2005|www.nature.com/nature 811
Figure 1 Cochlear amplification. a, The cochlea.
Sound hitting the eardrum is transformed into
vibrations of the middle ear bones. The smallest,
the stapes, couples the vibration into the cochlea.
The organ of Corti is found along the length of the
cochlea, sandwiched between two membranes;
which part vibrates depends on the frequency.
The cochlear amplifier increases and sharpens
the vibrations in response to soft sounds (blue
curve, passive vibration; red, cochlear amplifier
working). b, Cross-section through part of the
organ of Corti. Shearing between tectorial and
basilar membranes opens channels in the bundles
of outer hair cells, causing K+
and Ca2+
ions to
flow in.The cochlear amplifier in these cells (green
arrows, force generator in the hair bundle and/or
prestin protein in the cell membrane) enhances
the vibrations in different parts of the organ of
Corti (blue arrows, no amplification; red arrows,
amplifier active). This boosts the membranes'
motion and, via fluid coupling, the hair bundles
of the inner hair cells. Afferent nerve fibres
contact the inner hair cells and signal sound
reception to the brain; efferent nerve fibres allow
the brain to control outer hair cells.Arrows
indicate motion in the excitatory direction.
Low-frequency
end
High-frequency
end
Organ
of Corti
Outer
hair
cell
Ca2+
K+
Inner
hair
cell
Stapes
Tectorial
membrane
Ca2+
K+
Basilar membrane
a
b
Efferent
nerve
fibre
Afferent
nerve
fibre
displacement.Thiscalcium-dependentadap-
tation is extremely fast in mammalian outer
haircells9
,andmayhelpthemtorespondbest
to sound frequencies appropriate for their
positionalongthecochlearspiral.
This work shows that the hair bundles of
outer hair cells contain a fast force generator
that does not suffer from the speed limita-
tions of being voltage dependent. But could
itreallyprovideamplification invivo?Thisis
whereChanandHudspeth'sstudy2
comesin.
Their experimental approach was to take a
turn of the gerbil cochlea and put it in an in
vitro environment that painstakingly recre-
atedthenormal,invivo,situation.Itwasthus
possible to stimulate the organ of Corti with
sound and to record the motion of the hair
bundlesof theinnerhaircells.
Theauthorsobservedevidenceforampli-
fication of the bundle motion at low sound
intensities. The amplification disappeared
when the transducer current was pharmaco-
logicallyblocked.Thisbyitselfdoesnotprove
that the amplification is in the hair bundle:
no transducer current also means no recep-
tor potential and hence no prestin-driven
electromotility. However, when Chan and
Hudspeth then prevented most of the trans-
ducer current (normally carried by potas-
sium ions), just leaving the small fraction
that is carried by calcium ions, the receptor
potentials of the outer hair cells would have
been much attenuated (although these were
not measured). But the amplification in the
motion of the inner-hair-cell bundles
remained. The conclusion is that calcium-
dependent force generation by the outer-
hair-cell bundles may be sufficient to drive
the cochlear amplifier (Fig. 1b), without the
needforelectromotility.
So what of prestin? Genetically engi-
neered mice lacking this protein do not have
normal cochlear amplification, to which it
must therefore make some contribution10
.
Prestin might work at a more leisurely pace,
keeping the hair bundles at their most sen-
sitive position and mediating the brain's
ability to turn the noise down, through
activation of the nerve fibres that signal to
the outer hair cells. Perhaps it should be
renamed`andantin'.
These first demonstrations of force gen-
erationbythehairbundlesofouterhaircells1
and their effects on cochlear amplification2
were obtained with cells from the low-fre-
quency part of the cochlea,and it needs to be
shown that they also apply at the speed limit
of mammalian hearing. Other evidence is
still missing, too. Do the forces measured by
Kennedy and colleagues1
disappear when
transduction is blocked? Why do Chan and
Hudspeth's results2
not quite match the in
vivo performance, even at low frequencies?
What are needed now are experiments and
models that lead to a precise, quantitative
understanding of the balance of power
between prestin and hair-bundle forces in
cochlearamplification. 
Corné Kros is in the School of Life Sciences, University
of Sussex, Falmer, Brighton BN1 9QG, UK.
e-mail: c.j.kros@sussex.ac.uk
1. Kennedy, H. J., Crawford, A. C. & Fettiplace, R. Nature 433,
880­883 (2005).
2. Chan, D. K. & Hudspeth, A. J. Nature Neurosci. 8, 149­155 (2005).
3. Dallos, P., Popper, A. N. & Fay, R. R. (eds) The Cochlea
(Springer, New York, 1996).
4. Brownell, W. E., Bader, C. R., Bertrand, D. & de Ribaupierre, Y.
Science 227, 194­196 (1985).
5. Zheng, J. et al. Nature 405, 149­155 (2000).
6. Frank, G., Hemmert, W. & Gummer, A.W. Proc. Natl Acad. Sci.
USA 96, 4420­4425 (1999).
7. Santos-Sacchi, J. J. Neurosci. 12, 1906­1916 (1992).
8. van Netten, S. M. & Kros, C. J. Proc. R. Soc. Lond. B 267,
1915­1923 (2000).
9. Kennedy, H. J., Evans, M. G., Crawford, A. C. & Fettiplace, R.
Nature Neurosci. 6, 832­836 (2003).
10.Liberman, M. C. et al. Nature 419, 300­304 (2002).
Photonics
Expect more delays
Joe T. Mok and Benjamin J. Eggleton
Slow light research has been a fast-moving topic in recent years, with
potential applications from quantum computing to telecommunications.
Techniques are now emerging that can slow down light in optical fibres.
L
ight travels at a speed c of 300 million
metres per second in a vacuum, but
can be slowed down to cycling speed
(around 17 metres per second)1
or can even
be brought to a halt2,3
, when the right
medium is used. Although we may not see
commercial applications appearing imme-
diately, there is a clear potential for making
practical use of slow light. Recently, Song et
al.4
reported a technique to delay light in
optical fibres, aiming at applications in
fibre-optic communication networks.
An example of a device where slow light
could be particularly useful is an all-optical
router. Routers are used in communication
systemstodirectinformationfromonepoint
to another. Whereas today's routers function
by first converting the information sent in
optical form into electronic form, all-optical
routers use all-optical switching schemes,
eliminating the optical­electronic­optical
conversion and are therefore inherently fast.
The realization of an all-optical router
requires an optical buffer -- a component
that functions as temporary optical storage,
to effectively synchronize data packets. This
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