DOI: 10.1126/science.1204076
, 1262 (2011);333Science
, et al.Xiaoke Chen
A Gustotopic Map of Taste Qualities in the Mammalian Brain
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A Gustotopic Map of Taste Qualities
in the Mammalian Brain
Xiaoke Chen,1
Mariano Gabitto,1
Yueqing Peng,1
Nicholas J. P. Ryba,2
Charles S. Zuker1,3
*
The taste system is one of our fundamental senses, responsible for detecting and responding to
sweet, bitter, umami, salty, and sour stimuli. In the tongue, the five basic tastes are mediated
by separate classes of taste receptor cells each finely tuned to a single taste quality. We
explored the logic of taste coding in the brain by examining how sweet, bitter, umami, and salty
qualities are represented in the primary taste cortex of mice. We used in vivo two-photon
calcium imaging to demonstrate topographic segregation in the functional architecture of the
gustatory cortex. Each taste quality is represented in its own separate cortical field, revealing the
existence of a gustotopic map in the brain. These results expose the basic logic for the central
representation of taste.
T
he sense of taste is in charge of evaluating
the nutritional value of a meal. In
mammals, a very small palette of taste
qualities orchestrates appetitive responses to
energy- and protein-rich food sources (sweet
and umami) and warns against the ingestion of
toxic or spoiled/fermented foods (bitter and sour/
carbonated). Salt sensing aids the adequate consumption
of sodium while cautioning against the
ingestion of excess salt. The attraction toward
sweet, umami, and low-sodium, and the aversion
toward bitter, sour, and high-salt, is innate and
largely invariant throughout life. These observations
suggest a physiological hard-wiring of
tastant quality to hedonic value.
Each of the five basic tastes is detected by
specialized sensors expressed on receptor cells
of the tongue and palate epithelium (1–11). Over
the past 10 years, we have shown that each receptor
class is expressed in its own distinct taste
cell type (2–6, 8, 12, 13). This “one cell, one
taste” coding scheme is the hallmark of the organization
of the mammalian taste system at the
periphery, and is the mechanism through which
individual taste qualities are recognized and encoded
in the tongue (9, 14).
In rodents, information from taste cells in the
oral cavity is transmitted to the primary taste
cortex, the insula, through multiple neural stations
(14, 15). How are the chemical senses
represented in the cortex? Recent studies on the
representation of odors in the primary olfactory
cortex revealed a sparse and distributed pattern
of neuronal activity whereby each odor is encoded
by a unique ensemble of neurons, but
without any spatial clustering or preference in
relation to odorant space (16). This is in contrast
to the organization of the primary visual, somatic,
and auditory cortices, where neurons that
respond to similar features of the sensory stimulus
are topographically organized into spatial
maps in the cortex (17–19).
Previous studies examining how tastes are represented
in the primary gustatory cortex have
relied on a number of elegant approaches (20–25).
Unfortunately, these experiments have led to
inconclusive and often contradictory views of
the central representation of taste, in part because
of the limited spatial resolution of the techniques
and/or the shortfalls of recording from
small numbers of neurons (15, 26). We reasoned
that if one could simultaneously examine
the activity of large numbers of neurons in the
insular cortex in response to taste stimulation
(27), and do so with single-cell resolution, it
should be possible to determine how the tastes
are represented in the primary taste cortex.
Imaging gustatory responses in the primary
taste cortex. We used two-photon calcium imaging
(16, 28–30) to monitor tastant-evoked neural
activity across the gustatory cortex in vivo. To
confirm the appropriate region for imaging in
mice (20, 25), we used extracellular electrodes
to record tastant-evoked responses in the gustatory
area of the thalamus (Fig. 1), and after
identifying taste-responding cells, we used an
AAV2/hu11-GFP virus (31) as an anterograde
tracer to label (and trace) projections to the primary
taste cortex (Fig. 1C) (32). These studies
demarcated a domain of ~2.5 mm2
in the insula,
located ~1 mm above the intersection of the
middle cerebral artery (MCA; Fig. 1, A and C)
and the rhinal veins, and extending ~1 mm anteriorly,
1.5 mm posteriorly, and 1 mm dorsoventrally.
Small areas of cortex were exposed in
this region of the insula of anesthetized animals
(via surgical craniotomy), and the neurons were
bulk-loaded with the calcium-sensitive dye
Oregon Green 488 BAPTA-1 AM (OGB) for
functional imaging (Fig. 1D); this dye is effectively
taken up by the cells (fig. S1) and serves
as a robust fluorescent sensor of neural activity
with high signal-to-noise ratios (16, 29, 30). To
ensure that responses reflected biologically relevant
stimuli, we used concentrations of tastants
that reliably elicit ~80% of the maximal response
in behavioral studies (3, 8).
Representation of bitter taste. We systematically
inspected layer 2/3 of the gustatory cortex
(a layer readily accessible by two-photon
imaging) for tastant-evoked responses by parsing
and tiling the insula into fields of 350 mm ×
350 mm and testing for neurons that exhibited
correlated patterns of tastant-dependent firing
(16). The stimulus paradigm consisted of a prestimulus
application of artificial saliva for 30 s,
exposure to a test tastant for 10 s, and a poststimulus
artificial saliva wash for 30 s (32). We
began by focusing on bitter taste, and discovered
a highly localized, topographically defined
cluster (i.e., a “hot spot” at ~1 mm dorsal to the
rhinal veins and ~1 mm posterior to the MCA)
(32), where many neurons responded to bitter
stimuli with highly significant increases in intracellular
calcium (DF/F ranging from 20 to
65%; Fig. 2); the location of the hot spot was
stereotyped so that we could consistently find
this cortical field in multiple animals (Fig. 2F
and fig. S2). We examined the reproducibility of
the taste-evoked responses in the hot spot by
measuring variability across trials. We imaged
~200 neurons per trial, and these were segmented
and coded according to their location and response
magnitude (16, 33). On average, about
one-third of the OGB-labeled neurons fired
during the window of bitter tastant application,
and the vast majority of these (>70%) responded
in multiple bitter-stimulation trials (compare Fig.
2A and 2B; see also fig. S3). By examining bitter
responses across the entire gustatory cortex
in multiple animals, we confirmed this hot spot
(i.e., cortical field) as the only region that exhibited
correlated responses to bitter stimuli (Fig.
2F and fig. S2).
Are the bitter-responsive neurons selective or
broadly tuned? We recorded from the bitter hot
spot while stimulating the tongue with tastants
representing the different taste qualities. Bitterresponding
neurons were exquisitely tuned to
bitter, with no other taste quality represented in
this spatial domain of the gustatory cortex (Fig. 2).
Equivalent results were obtained in single-unit
electrophysiological recordings from within the
bitter hot spot (fig. S4).
Humans and rodents recognize a wide range
of bitter tasting chemicals, and their genomes
correspondingly include a large number of genes
that encode bitter taste receptors (T2Rs) (5–7).
Most, if not all, T2Rs are expressed in the same
subset of taste receptor cells (5), implying that
these cells act as broadly tuned bitter sensors capable
of detecting a wide range of bitter-tasting
chemicals (5, 8). Thus, we predicted that the cortical
representation for different bitter tastants
should be shared. We therefore assayed the responses
to several chemically distinct bitter tastants,
and indeed all of them activated the same hot
spot (Fig. 3 and fig. S3).
Specificity of cortical responses to taste
stimuli. To further validate the specificity of the
bitter cortical field, we examined taste responses
in engineered mice where a single one of the
1
Howard Hughes Medical Institute, Department of Biochemistry
and Molecular Biophysics, and Department of Neuroscience,
College of Physicians and Surgeons, Columbia University,
New York, NY 10032, USA. 2
National Institute of Dental and
Craniofacial Research, Bethesda, MD 20892, USA. 3
Departments
of Neurobiology and Neurosciences, University of California,
San Diego, La Jolla, CA 92093, USA.
*To whom correspondence should be addressed. E-mail:
cz2195@columbia.edu
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bitter taste receptors had been eliminated. T2R5
is one of the 36 bitter receptors in the mouse
genome (34); it is necessary (and sufficient) for
physiological and behavioral taste responses to
the toxin cycloheximide, but not for detecting a
wide range of other bitter chemicals (6, 8). If the
bitter-evoked activity in the hot spot is indeed
used to represent bitter taste, then all responses
to cycloheximide should be missing in a T2R5
knockout (T2R5-KO) animal. However, responses
to other bitter tastants should remain.
This selective-loss experiment alleviates the uncertainty
associated with examining animals with
a total loss of bitter taste [e.g., TRPM5 or PLCb2
knockouts (13)], as such a negative result could
not be distinguished from a trivial failure to
record cortical responses. As predicted, cycloheximide
responses were abolished in the bitter
hotspot of T2R5-KO animals, but responses to
other bitter chemicals were indistinguishable from
those in control mice (Fig. 3).
A spatial map of taste qualities. Given the
existence of a topographically defined region for
the representation of bitter taste, we hypothesized
that sweet taste would also be encoded
in its own cortical field, and therefore surveyed
the insular cortex for selective activity to sweet
tastants. We discovered such a specific sweet hot
spot at a considerable distance from the bitter hot
spot (~2.5 mm rostrodorsal to the bitter field;
Fig. 4, A and B). There, a large ensemble of
neurons responded to sweet taste stimulation
of the tongue. Multiple lines of evidence validate
that area as the sweet cortical field: First, the cells
were preferentially tuned to sweet taste versus
any of the other taste qualities (Fig. 4B and fig.
S5). Second, the very same hot spot was activated
by structurally different sweet-tasting chemicals
(e.g., artificial versus natural sweeteners),
but not by tastants for other taste qualities (Fig. 4,
A and B, and fig. S5). Third, responses were
abolished in sweet-receptor knockout animals
[T1R2-KO (3); fig. S6]. Finally, this is the only
region of gustatory insula that showed correlated
activity in response to sweet taste.
The topographic separation of sweet and
bitter taste into distinct and nonoverlapping
gustatory fields in the primary taste cortex reveals
the existence of a functional “gustotopic
map.” In the other chemosensory modality, olfaction,
individual odorants are represented in
the primary olfactory cortex by the activation of
spatially dispersed ensembles of neurons, without
any discernible topographic or chemotopic
organization (16). However, unlike the olfactory
system—which must recognize, distinguish, and
often initiate distinct physiological and behavioral
responses to a vast universe of chemically
distinct odorants—the chemical-perceptual space,
represented by the five basic taste qualities, is
remarkably limited (9, 14). Sweet and bitter
exemplify the two poles of the gustatory spectrum;
thus, we wondered whether the other taste
qualities were also part of a gustatory map in
the insula.
Umami is the savory taste that humans
associate with monosodium glutamate (MSG);
most other mammalian species use the umamisensing
taste receptor cells to recognize and mediate
appetitive responses to protein-rich food
sources [e.g., the taste of all amino acids (1, 2, 35)].
We searched the insular cortex for umami-evoked
neuronal activity by stimulating the tongue with
monopotassium glutamate (36). Indeed, just as
seen for bitter and sweet, the cortical representation
of umami was also part of the gustotopic
map, with a unique hot spot for umami taste
(Fig. 4, C and D, and fig. S5). The umami cortical
field was specifically tuned to umami versus the
other four taste qualities. As expected, this hot
spot was activated by other L-amino acids (e.g.,
umami agonists; Fig. 4D) but not by their enantiomeric
inactive D-forms (2, 3).
The remaining two basic tastes, salt (sodium)
and sour (acid) sensing, are mediated by ion
channel receptors rather than by G protein–
coupled receptors (10–12, 37). Does the same
organization apply to ionic tastes? Our efforts to
uncover an acid (sour) hot spot did not succeed.
We believe this could be because its location
was outside the area sampled in our studies, or
even because acid stimuli also act on a number
of other pathways, such as pain and somatosensation
(38), possibly leading to changes in its
cortical representation. Thus, we focused on sodium
taste.
Low concentrations of NaCl (i.e., appetitive
salt taste) are sensed by a unique population of
taste receptor cells via the ENaC ion channel
(12). A salient feature of this response is its
inhibition by amiloride and its strong selectivity
for sodium versus other salts (12). Therefore,
we searched for a salt-responsive cortical
B
40
20
0
Spikes/s
Sucrose
0
D
C
10 s
MCA
RV
A
LOT
Fig. 1. Two-photon imaging in the mouse insular cortex. (A) Photograph of a mouse brain highlighting
the approximate location of our imaging studies in the primary taste cortex (yellow). Also shown are the
superimposed drawings of two key vascular landmarks (MCA, middle cerebral artery; RV, rhinal vein;
LOT, lateral olfactory tract). (B) Responses of a sweet-sensitive thalamic taste neuron to 300 mM
sucrose; the box indicates the time and duration of the sweet stimulus. After identification of such tasteresponsive
neurons, cells around the recording site were infected with an AAV2/hu11-GFP virus to label
their terminal fields in layer 4 of the gustatory cortex. (C) Coronal section of a mouse brain (bregma +1.0)
stained with TO-PRO-3 (red). Shown is the location of the thalamocortical projections labeled after
infection with the AAV2/hu11-GFP virus (white box). To triangulate this region in relation to the vascular
landmarks, we injected 1,1´-dioctadecyl-3,3,3´,3´-tetramethylindocarbocyanine perchlorate (DiI) at
the intersection between the RV and the MCA (pseudocolored in blue; solid arrow) and at 1 mm
above (open arrow). (D) Images of bulk-loaded neurons and astrocytes in layer 2/3 of the primary
gustatory cortex (see also fig. S1) stained with Oregon Green 488 BAPTA-1 AM (green fluorescence)
and sulforhodamine 101 (yellow-labeled astrocytes). Animals were imaged using two-photon microscopy
in vivo after surgical craniotomy. Scale bars, 1 mm [(A) and (C)], 100 mm (D).
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cluster that met those criteria. Just as shown
for the other basic taste qualities, sodium taste
is also represented in its own spatially segregated
field (Fig. 4, E and F, and fig. S5). The
responding neurons are exquisitely tuned to
NaCl versus the other taste qualities, are sensitive
to amiloride, and are specific for sodium
versus other cations (e.g., KCl, MgCl2).
Concluding remarks. For many years, the
prevailing views about the organization and function
of the taste system at the periphery centered
around the concept of taste coding via broadly
tuned taste receptor cells (39–41). Individual taste
receptor cells were proposed to express receptors
for various taste qualities and thus respond to
multiple taste stimuli. Now, however, we know
that each of the five basic tastes is mediated by
its own class of taste receptor cells, each tuned
to a single taste quality, thus defining a “one cell,
one taste” coding logic (9, 14). Notably, existing
models of taste coding in the insula included
proposals of broadly tuned neurons across taste
qualities [with no spatial segregation (15)], as
well as others suggesting a certain degree of
topographic organization, but with no region
dedicated to the processing of only one taste
quality (20, 25, 26). Although we cannot rule out
the existence of sparse numbers of broadly tuned
cells (24, 26) distributed throughout the taste
cortex (i.e., nonclustered), our results reveal that
Bitter
Sour
Salt
Sweet
AS
30
20
10
0
Respondingcells(%)
c
50% ∆F/F
G
80
0
40
500 25
∆F/F(%)
Cell #
SweetCBitterA B Bitter D Sour
E
H
Bitter
Sour
Sweet
Salt
F
R
VBitter
Fig. 2. Tastant-evoked responses in the bitter hot spot. (A) Bitter tastant stimulation of the tongue (single
trial) evoked robust responses in the bitter hot spot. The image illustrates changes in OGB fluorescence in
response to a 1 mM cycloheximide stimulus; ~35% of the loaded neurons responded with ∆F/F greater
than 3.5 standard deviations above background (red cells; see also fig. S7). (B to D) In contrast to the
sparse activity seen during application of other tastants [(C) and (D); see text], neurons activated by bitter
tastant responded over multiple trials; cells that responded in at least two of four trials are labeled white
(B). (E) Neurons in the bitter hot spot responded selectively to bitter versus other taste stimuli (n = 8). AS,
artificial saliva. (F) An illustration and a bright-field image depicting the approximate relation of the bitter
cortical field (solid red circle) to the vascular landmarks; the dotted circles depict the location of the bitter
hot spot in four additional animals (32). The middle panel has been flattened to present a twodimensional
view of this area of the brain. (G) Bitter-responsive neurons are highly tuned to bitter taste
(red). The graph shows the rank-ordered ∆F/F of a set of bitter-responsive neurons in a six-trial experiment
to bitter stimuli versus other tastants (bitter = 1 mM cycloheximide; NaCl = 100 mM NaCl; sweet =
30 mM acesulfame K; sour = 10 mM citric acid). No apparent organization according to response
amplitude was seen within the cluster (fig. S8). (H) Representative changes in OGB fluorescence during
bitter (red), sweet (green), and sour (blue) stimulation for 10 s. Scale bars: 100 mm [(A) to (D)], 0.5 mm
(F); error bars are means T SEM.
T2R5-KOControl
QuinineCycloheximideAceK
A B
C D40
20
0
Respondingcells(%)
Quinine
Cyclohexim
ide
AceK
Quinine
Cyclohexim
ide
AceK
Fig. 3. Responses in the bitter hot spot are dependent
on bitter taste receptor function. (A) Different
bitter compounds activate the same hot spot
in the cortex (see fig. S3) (n = 4). (B) Animals lacking
the bitter taste receptor for cycloheximide (T2R5-KO)
selectively lack cortical responses to cycloheximide
but retain normal responses to other bitters (e.g.,
10 mM quinine) (n = 2, seven trials per tastant). (C
and D) Quantitation of taste responses in the control
and T2R5-KO animals; also shown are data for
a sweet tastant (acesulfame K). Note the lack of
responses in both controls (C) and KO animals (D).
Scale bars, 100 mm; error bars are means T SEM.
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the individual basic tastes are represented in the
insula by finely tuned cells organized in a precise
and spatially ordered gustotopic map, where each
taste quality is encoded in its own (segregated)
stereotypical cortical field.
The organization of the primary taste cortex
appears at first glance to be reminiscent of the
somatosensory, auditory, and visual systems,
which exhibit spatially organized somatotopic,
tonotopic, and retinotopic cortical maps (17–19).
However, the cortical maps for these three sensory
modalities reflect smooth transitions across
features of sensory space, whereas this is not
the case in the taste system. Furthermore, in the
somatosensory, auditory, and visual systems, the
peripheral receptors display exacting spatial order,
whereas in taste, a distributed ensemble of peripheral
receptor cells in the tongue—without any
spatial organization, but with defined identities—
nonetheless converge into a fixed cortical map
where neurons with similar response profiles are
clustered. Why should taste be represented in a
spatial map? We speculate that this organization
has an ancient evolutionary, possibly developmental,
origin rather than a strictly functional
origin. Indeed, the perceptual space to be represented
by the taste system is limited to just a
handful of qualities; thus, having each basic
taste represented in individually segregated fields
provides a simple and elegant architectural solution
to pattern, wire, and interconnect the ensembles
of neurons representing each taste quality.
Our studies suggest that the cortical fields
representing the individual basic tastes cover only
a small fraction of the insula. What does the rest
of the insula do? We found that outside the hot
spots, only small numbers of sparsely distributed
neurons exhibited significant changes in fluorescence
during the window of tastant presentation
(fig. S6; see also fig. S4). The same results were
observed in animals lacking taste receptor function
(fig. S6) and irrespective of the quality of
the taste stimulus (including artificial saliva
alone); hence, these changes apparently do not
represent responses to the individual basic tastes.
Therefore, the inter–hot spot regions might be
involved in other aspects of taste coding, such as
the representation of taste mixes, and thus may
Fig. 4. The basic tastes are
represented in a spatial map in
the primary taste cortex. (A
and B) Sweet taste is represented
in its own cortical field
(solid green circle), ~2.5 mm
rostrodorsal from the expected
location of the bitter hot spot
(red circle in upper left illustration).
Also shown is the
location of the sweet hot spot
in three additional animals
(open green circles). (A) About
35% of the OGB-labeled neurons
in the sweet cortical field
respond in multiple trials to
sweet taste stimulation of the
tongue (green-labeled neurons),
but not to other tastes
(e.g., bitter and sour). (B) The
responses are highly specific
for sweet tastants (see also fig.
S7), including natural and artificial
sweeteners. (C) Umami
taste is also represented in its
own stereotypical hot spot,
found ~1 mm caudal and ventral
to the expected sweet
cortical field (yellow circle).
(D) Responses are selective for
umami tastants, including various
L-amino acids, but not to
D-amino acids or other taste
qualities. (E) Low concentrations
of sodium salt (100 mM
NaCl) are known to activate a
unique population of sodiumsensing
taste receptor cells (12)
and are represented in a distinct
cortical field (orange circle)
~1 mm equidistant from
the expected sweet and umami
hot spots. (F) Amiloride completely
abolishes both the function
of the sodium taste receptor
and the insular representation of sodium taste. Other salts do not activate
the sodium sensor (12) and indeed are not represented in the sodium hot
spot (e.g., KCl, MgCl2). See fig. S5 for additional details on the sweet,
umami, and sodium responses. Scale bars, 100 mm (0.5 mm in the cortex
diagrams); error bars are means T SEM. The hot spots for the different
tastes are too far from each other to be imaged on the same animal;
reconstructions are based on multiple animals. A minimum of four animals
and four trials per animal/per tastant were used to define the sweet (n = 10
animals), umami (n = 5 animals), and sodium (n = 4 animals) cortical
fields.
R
V
Bitter
Sweet
Umami
D
F
30
20
10
0
Respondingcells(%)
Bitter
Sour
AS
Sweet
Um
am
i
L-Ser
D-Trp
NaClBitter
Sour
AS
NaCl
Sweet
30
20
10
0
Respondingcells(%)
NaCl+
am
iloride
M
gCl2
KCl
B Sweet
Bitter
NaCl
Sour
AS
30
20
10
0
Respondingcells(%)
Sucrose
AceK
Sweethotspot
A
Sweet
Sour
Bitter
UmamihotspotNaClhotspot
C
NaCl
Sweet
Umami
R
V
Bitter
SweetNaCl
Umami
E Sweet
Bitter
NaCl
R
V
Bitter
Sweet
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help to code the perception of “flavor” [e.g.,
responding to several tastes simultaneously
(24, 26, 42)]. In addition, the insular cortex responds
to more than just taste, and it is often
thought of as a site for multisensory integration
(15, 42, 43). Thus, these areas may participate in
the integration of taste with the other senses.
The discovery of a gustotopic map in the
mammalian cortex, together with the advent of
sophisticated genetic and optical tools (44), should
now make it possible to experimentally manipulate
the taste cortex with exquisite finesse.
In future studies, it will also be important to
elucidate how taste intensity is encoded in the
insular cortex, and to determine whether taste
qualities with similar valence project to common
targets. Likewise, tracing the connectivity
of each of the basic taste qualities to higher brain
stations will help decipher how these integrate
with other modalities and combine with internal
and emotional states to ultimately choreograph
taste behaviors (45).
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Acknowledgments: We thank A. Devor and Y. Dan for their
hospitality and technical help with our early intrinsic imaging
attempts, R. Barreto for valuable help with imaging and
data analysis, S. Hunter-Smith for help with viral tracing
experiments, and R. Axel, K. Scott, D. Steddler, R. Bruno, and
members of the Zuker lab for helpful comments. Supported
by a Human Frontier Science Program fellowship (X.C.) and by
the Intramural Research Program of the National Institute of
Dental and Craniofacial Research. C.S.Z. is an investigator of
the Howard Hughes Medical Institute.
Supporting Online Material
www.sciencemag.org/cgi/content/full/333/6047/1262/DC1
Materials and Methods
Figs. S1 to S8
References
9 February 2011; accepted 8 July 2011
10.1126/science.1204076
REPORTS
Vacuum-Induced Transparency
Haruka Tanji-Suzuki,1,2
* Wenlan Chen,2
Renate Landig,2
Jonathan Simon,1
Vladan Vuletić2
Photons are excellent information carriers but normally pass through each other without
consequence. Engineered interactions between photons would enable applications as varied as
quantum information processing and simulation of condensed matter systems. Using an ensemble
of cold atoms strongly coupled to an optical cavity, we found that the transmission of light through
a medium may be controlled with few photons and even by the electromagnetic vacuum field. The
vacuum induces a group delay of 25 nanoseconds on the input optical pulse, corresponding to a
light velocity of 1600 meters per second, and a transparency of 40% that increases to 80% when
the cavity is filled with 10 photons. This strongly nonlinear effect provides prospects for advanced
quantum devices such as photon number–state filters.
T
he experimental realization of strong coherent
interactions between individual
photons will enable a variety of applications
such as quantum computing (1–3) and
studies of strongly correlated many-body quantum
systems (4). Two main approaches to generating
photon-photon interactions are strong
coupling of single emitters to optical cavities
(2, 3, 5–9) and electromagnetically induced transparency
(EIT) in ensembles of atoms (10–12).
Single emitters strongly coupled to cavities can
provide substantial optical nonlinearity at the
expense of typically large input-output coupling
losses and the technical challenges of trapping
and manipulating single particles. EIT in atomic
ensembles provides an impressive degree of coherent
control in simple, elegant experiments
(12–15), but the nonlinearities achieved so far
are relatively weak, requiring (for example) ~500
photons for all-optical switching (16). We demonstrate
that by using an optical cavity to enhance
the EIT control field, the resonant transmission
of light through an atomic ensemble can be substantially
altered by a few photons and even by
the cavity vacuum (17, 18). Because the effect
is nonlinear in both control and probe fields at
the single-photon level, it should enable advanced
quantum optical devices such as photon
number–state filters (19) and nondestructive
photon number–resolving detectors (20, 21).
We call the limiting case with no photons initially
in the cavity “vacuum-induced transparency”
(VIT) (17) to distinguish it from recent
cavity EIT demonstrations using a single atom
with cavity-enhanced absorption and a classical
control field containing many photons (22, 23).
In contrast, VIT may be realized with only one
photon in the entire system.
We experimentally realize Field’s original proposal
(17) to replace the EIT control field by
the vacuum field inside a strongly coupled cavity
(Fig. 1). In an atomic L system | f 〉 ↔ |e〉 ↔ |g〉
with two stable states |f 〉, |g〉, the probe beam
addresses the |f 〉 → |e〉 transition, whereas the
cavity mode is tuned near the |g〉 → |e〉 transition.
A cold atomic ensemble is prepared in the state |f 〉
by optical pumping. VIT for the probe beam can
be thought of as arising from a vacuum-induced
Raman process where the incoming probe photon
is absorbed, quickly emitted into the cavity,
then reabsorbed by the ensemble and reemitted
1
Department of Physics, Harvard University, Cambridge, MA
02138, USA. 2
Department of Physics, MIT-Harvard Center for
Ultracold Atoms, and Research Laboratory of Electronics, Massachusetts
Institute of Technology, Cambridge, MA 02139, USA.
*To whom correspondence should be addressed. E-mail:
haruka.tanji@post.harvard.edu
2 SEPTEMBER 2011 VOL 333 SCIENCE www.sciencemag.org1266
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