Available online at www.sciencedirect.
com
Gain control mechanisms in the auditory pathway
Benjamin Louis Robinson and David McAlpine
Belying the apparent ease with which the acoustic world is
perceived, the sheer vastness of the range of sounds and
sound parameters that must be encoded represents a
challenge to traditional models of neural coding in audition.
Here, we review recent evidence suggesting that a process of
gain control, operating at multiple stages in the auditory
pathway, helps maintain coding accuracy to prevailing sound
conditions over a wide range of behavioural and sensory
contexts. Together, these processes imbue the system with its
staggering representational capacity, underpinning everything
from the perception of a tiger’s near-silent tread to its
triumphant roar, demonstrating once more the principle of
efficient coding that underlies sensory processing.
Address
UCL Ear Institute, 332 Gray’s Inn Road, London WC1X 8EE, UK
Corresponding author: McAlpine, David (d.mcalpine@ucl.ac.uk)
Current Opinion in Neurobiology 2009, 19:402–407
This review comes from a themed issue on
Sensory systems
Edited by Leslie Vosshall and Matteo Carandini
Available online 6th August 2009
0959-4388/$ – see front matter
Published by Elsevier Ltd.
DOI 10.1016/j.conb.2009.07.006
Introduction
The environment imposes two conflicting demands upon
sensory systems. On the one hand, natural signals are often
of extremely small magnitude, favouring the evolution of
sensory systems with high sensitivity [1]. On the other
hand, the range over which these signals varies is anything
but small: the difference between a whisper and a roar, for
example, is 10 or 12 orders of intensity [2]. Given biological
constraints, how do sensory systems cope with the simul-
taneous requirements of high sensitivity and accuracy over
a wide dynamic range? A possible solution to the conflicting
demands of sensitivity and accuracy lies in the imple-
mentation of gain control, a solution variously instantiated
throughout many sensory systems, including the auditory
system. Strictly, the term ‘gain’ refers to the slope of an
input–output function, and it is well established that a
neuron’s response or output gain can be rapidly adjusted in
a process referred to as divisive normalisation [3]. However,
the evident complexity of any relationship between intra-
cellular, sub-threshold activity and spike generation
suggests that, for purely technical reasons, it is not always
Current Opinion in Neurobiology 2009, 19:402–407
possible to distinguish changes in gain from other changes
that influence neural output functions, especially when
relying on extracellularly recorded neural data to make
such distinctions [4]. What has become clear, however, is
that changes in gain often imply neural adaptations that
result in the recoding of sensory information according to
current environmental demands.
Here, we review recent evidence demonstrating the
importance of gain control in the auditory pathway —
and the adaptive recoding such gain control implies —
from the external surface of the ear to the primary
auditory cortex. We propose that the multiple time-
courses over which changes in neural gain are imple-
mented, as well as the burgeoning number of candidate
effectors of gain change, challenge the traditional means
of assessing auditory coding using relatively low-level
acoustic cues. What emerges is an exquisite degree of
coding control fitted to the stimulus context, even at very
early stages of neural processing [5].
Gain and the peripheral auditory system
Aside from its protective function, the outer ear performs at
least two significant acoustic functions in hearing. Not only
does its complex geometry provide for a frequency-de-
pendent increase (or decrease) in sound energy reaching
the eardrum, but also this transformation in sound energy
(the head-related transfer function or HRTF) affords the
means by which sound-sources in the vertical plane are
located, including the ability to distinguish sources to the
front from those to the back [6]. In a clever demonstration
of the auditory brain’s sensitivity to the spatial cues pro-
vided in the HRTF, Hofman et al. [7] found that by altering
the shape of the outer ear with prosthetic molds they could
modulate the extent to which human listeners were able to
identify the location of the source of a sound along the
vertical dimension. Within a matter of weeks, however,
subjects chronically fitted with outer ear prostheses had
adapted to their new auditory cues, and were once more
able to distinguish sources above the horizon from those
below, indicating a significant recoding of the brain’s
representation of the surface of the external ear. This,
relatively long-term, process of adjustment clearly impli-
cates even the most peripheral components of the sensory
end organs in gain control. Interestingly (and unlike the
effect of employing prisms to adjust visual spatial cues),
upon removal of the prostheses, subjects were found to
have retained normal sensitivity to the original acoustic
cues generated by their own ears.
A more rapid means by which the auditory system demon-
strates the influence of gain lies in the process of sensory
www.sciencedirect.com
 Gain control mechanisms in the auditory pathway Robinson and McAlpine 403
transduction that occurs at the level of the cochlea of the
inner ear. Transmission of sound energy via the bones of
the middle ear (themselves subject to a form of input gain
control through the action of the middle-ear reflex) to the
oval window of the cochlea generates a travelling wave
along the coiled basilar membrane. Current investigations
focus on understanding cellular mechanisms underlying
particular properties of basilar membrane responsiveness,
including the appearance of high gain at low intensities,
reduced, or compressive, gain responses at mid-intensi-
ties to high-intensities, and the contribution of these gain
mechanisms to the basilar membrane’s sharply tuned
frequency response — none of which is present in the
passive properties of the membrane (see [8]). These
changes in gain, important in themselves, accrue further
interest in that they are thought to underlie certain
psychophysical phenomena (see below). So what is it
that provides the cochlea with its boost in sensitivity?
The likely candidates, the outer hair cells (OHCs), out-
number the primary auditory transducers, the inner hair
cells (IHCs), by three to one, and appear to increase
cochlear gain by rapidly changing somatic length, thereby
altering the micromechanical properties of the basilar
membrane, rather like springs of adjustable tension
attached to the edges of a trampoline. In this way, the
travelling wave undergoes an overall amplification, a
compression at high levels and a sharpening at the
particular region of the basilar membrane representing
the frequency of the incoming sound. Recent research has
focused on the precise mechanism by which OHCs feed
energy back into the basilar membrane [9]. The details of
this mechanism are beyond the scope of the present
discussion and have been recently reviewed [10,11].
Gain control in the auditory midbrain
With its active elements intact, the dynamic range of the
cochlear input–output function matches well with psy-
chophysical data indicating that listeners are able to
distinguish changes in sound level in the order of 1
decibel (dB) or so over the full 120 dB range of human
hearing. This includes the existence of a ‘mid-level’
hump in discrimination performance — a reduction in
sensitivity over the range of sound levels where cochlear
compression is greatest [12]. In this context, therefore,
measurements of single ANFs, as well as in the midbrain
and cortex, have tended to reveal a somewhat surprising
picture. Typically, increases in neural spike-counts are
reported to extend over only the first 20–30 dB beyond
threshold before they reach rate saturation. Given that the
vast majority of ANFs show thresholds close to 0 dB
sound pressure level (SPL) — elevated threshold gener-
ally indicates some form of pathology — the possibility
that ANFs represent sound level in the form of a rate code
was disputed until only very recently. The ‘dynamic-
range problem’, a term coined to express this apparent
mismatch between psychophysical and neural perform-
ance, suggests an essentially static auditory system, one in
www.sciencedirect.com
which response functions at the earliest level of neural
coding in the auditory pathway are fixed in their repres-
entation of the acoustic environment, suited to detecting
and discriminating low-intensity sounds, but incapable of
distinguishing sounds at moderate or high levels. Indeed,
only recently was it suggested that sound level could not
be realised through a spike-rate code alone, and that other
forms of information (e.g. temporal) must play a role in
encoding sound level at the earliest neural stage of
processing. More recent studies, however, suggest that
the dynamic-range problem is simply the outcome of
employing a form of acoustic stimulation in physiological
studies that does not take full account of psychophysical
or natural listening conditions.
Motivated by studies of contrast gain control in the visual
system demonstrating the means by which neurons with
relatively small neural dynamic ranges can encode
changes in contrast extending over many orders of mag-
nitude, Dean et al. [13] assessed responses of neurons in
the auditory midbrain nucleus of the inferior colliculus
(IC) to a novel stimulus configuration. Hypothesising that
adaptation might result in alterations to coding of sound
intensity at the single-neuron level, these authors
recorded responses of individual IC neurons to continu-
ous wide-band noise whose level was adjusted every
50 ms to a value drawn from a statistical distribution,
defined by a high-probability region (HPR) from which
the majority (80%) of sound levels were drawn. When the
HPR was shifted to a new value, neurons’ spike-rate-
versus-level functions also shifted to accommodate the
new stimulus distribution, response functions continuing
to shift ‘rightwards’ as the HPR was shifted to higher and
higher levels. Moreover, as a population, neurons adapted
their response functions so as to maximise the accuracy
with which sound levels just above the background mean
were encoded. Neurons were found to adjust their coding
to new sound-level regimes within a few hundreds of
milliseconds [14]. In this case, changes in gain are mani-
fest as a precise and rapid reconfiguration of the relation-
ship between the input sound level and the neural
output — an adaptive recoding — to maximise the pre-
cision with which the sound environment is represented
by the auditory system. With recent conference reports
now indicating adaptive recoding to be a feature of the
responses of primary nerve fibres, the notion of a
dynamic-range problem in hearing has been much dimin-
ished. What was previously considered a coding problem
is now recognised as having constituted a limitation in our
understanding of how the brain represents infor-
mation — a limitation based on previously standard
laboratory technique that dictated that sounds be pre-
sented in pseudo-random order, with long intervals be-
tween successive presentations in order to lessen the
presumed malign influence of any adaptive mechanisms
on the proposed neural representation of intensity.
Released from this constraint, the auditory brain’s ability
Current Opinion in Neurobiology 2009, 19:402–407
404 Sensory systems
to extract information about the sound environment
effectively and efficiently, became evident [15]. Recent
psychophysical evidence supports these findings [12]:
Pienkowski and Hagerman measured intensity discrimi-
nation in listening conditions selected so as to prevent
central mechanisms of adaptation from having any useful
effect on the representation of sound level. They did so
by keeping sounds very brief (4 ms), and by employing
sequences of sounds widely separated in level. The data
from this study are striking: without central adaptive
mechanisms, intensity discrimination worsens signifi-
cantly at mid-range levels. The authors invoke cochlear
mechanisms to explain this so-called ‘mid-level hump’,
suggesting that the mid-range compressive non-linearity
in the cochlear response, described above, is a limiting
factor in sound-level discriminability across this range.
Central mechanisms, and then operating only for stimuli
of sufficient duration, are required to overcome this
decrement in performance for mid-level sounds. This
illustrates a remarkable point: it appears that peripheral
gain changes are necessary to allow the auditory system to
embrace as wide a range of levels as possible, but this
compression leads to a potential loss of accuracy; how-
ever, subsequent, central changes in gain — such as those
seen by Dean and colleagues — may largely compensate
for these necessary peripheral losses.
Cortical gain
We began by proposing gain as a possible solution to the
problems inherent in sound perception, namely the need
to encode small changes accurately over a large range of
sound intensities, including the very quiet. As suggested
above, the cochlea and sub-cortical auditory brain struc-
tures appear to address these problems to a great degree,
and it might therefore be reasonable to ask, in terms of
gain control, what role is left for the cortex if its inputs are
already well-matched to the statistics of incoming sound
stimuli? It should come as no surprise that cortical
neurons are in fact subject to significant changes in both
the gain and the form of their receptive-field properties,
and that these changes are initiated by a remarkable range
of sensory and non-sensory factors that, taken together,
provoke a profound reconsideration of the notions of
compression and dynamic range described for lower brain
centres.
Before discussing purely cortical forms of gain control, it
is important to note that some forms of gain control are
similar in sub-cortical and cortical brain centres. For
example, Phillips and Hall [16] report that rate-versus-
level functions for pure tones shift to higher levels when
presented against background noise. Rees and Palmer
[17] observe similar shifts sub-cortically, in the IC. These
shifts may aid the neural population in responding to
important sounds in noisy environments, such as picking
out a voice at a cocktail party. However, the possible
coding implications have not been explicitly examined on
Current Opinion in Neurobiology 2009, 19:402–407
a population level, rendering the functional implications
of these studies less clear than those of Dean et al. [13].
The range of shifts may share certain mechanisms; how-
ever, these changes in tone-evoked rate-versus-level
functions are thought to be due in part to cochlear
two-tone suppression — a very rapid mechanism that is
unlikely to contribute to the data of Dean et al., who
employed wide-band noise as a stimulus [13]. Further,
adaptation of the type seen by Dean et al. operates over a
time-scale of hundreds of milliseconds, well beyond the
temporal reach of two-tone suppression [14]. This brief
comparison illustrates the idea that gain control is useful
as a phenomenological description, but that mechanisms
and functions are likely to be manifold.
Given this complexity, it is important to try and establish
clear links between mechanistically similar forms of gain
control at different levels of the brain. Indeed, adaptation
resulting from the wide-band stimulus used by Dean et al.
in the IC has been examined explicitly in the cortex by
Watkins and Barbour [18], who reported an additional
feature of neural adaptation to sound-level statistics in
cortical neurons to that reported for IC neurons. A unique
feature of intensity coding in the auditory system is the
appearance of non-monotonic rate-versus-intensity func-
tions. Absent at the level of the auditory nerve, the
proportion of non-monotonic functions increases at sub-
sequent stations in the ascending pathway, such that by
the level of primary auditory cortex, fully half of neurons
exhibit some form of tuning for sound intensity. Cortical
neurons were found to respond in a manner that pre-
served coding accuracy for quiet sounds, even in the
context of a stimulus comprising mainly high sound
levels. Essentially, high sound levels lead to few if any
spikes being evoked in these neurons, rendering them in
a relatively un-adapted state. Low sound levels evoke
neural activity that, whilst maladapted to the high levels
in the underlying statistical distribution, is well placed to
encode the appearance of quiet sounds within the distri-
bution. The cortex therefore prevents adaptive recoding
occurring in some neurons in loud environments, to
preserve responsiveness to the sudden appearance of
quiet sounds.
In addition to such stimulus-driven changes in gain, cor-
tical neurons appear sensitive to non-sensory effectors of
gain change in their representation of complex sounds.
One of these effectors appears to be behaviour itself. In a
powerful demonstration of the effects of task-related
receptive-field changes, Fritz et al. [19] measured spec-
tro-temporal receptive fields (STRFs; time-dependent
and frequency-dependent receptive fields) of primary cor-
tical neurons in ferrets trained to perform an auditory
detection task. Neural STRFs were derived before, during
and following training periods in which animals were
required to detect the substitution of a complex broadband
sound with a pure tone. Remarkably, individual STRFs
www.sciencedirect.com
 Gain control mechanisms in the auditory pathway Robinson and McAlpine 405

were mutable during the behavioural testing, particularly
for frequencies at or close to that of the test tone. In general,
Fritz et al. found facilitation in STRF frequencies close to
the target frequency, changes which were swift in onset
and, in some cases, lasted for many hours. Whilst the power
normalisation procedure employed in this study precludes
any clear differentiation between changes in STRF gain
and changes in receptive-field shape, the results do suggest
highly localised increases in gain close to the tone fre-
quency, and decreases away from it. The link between
behaviour and STRF change was further demonstrated by
the observation that the magnitude of changes was corre-
lated with task performance — better performance equat-
ing with larger changes in the gain and shape of receptive
fields close to the frequency of the target tone. Further
studies by the same laboratory have extended these find-
ings to reveal a host of factors that evoke plasticity in
cortical receptive fields, including the type of task under-
taken (detection versus discrimination [20]), task difficulty
(high versus low signal-to-noise [21]) and stimulus com-
plexity (single versus complex tones [22]). Overall, a
picture is emerging indicating that auditory cortical
neurons can rapidly adjust their gain and reconfigure their
receptive-field properties in response to the moment-to-
moment demands of the sensory–motor milieu. Research
in species other than the ferret, and from other laboratories,
supports this notion, demonstrating a range of effects from
pure stimulus-driven gain changes [23–25] to alterations in
A1 receptive fields induced by self-stimulation of cortical
pleasure centres [26]. To summarise, it appears that gain
changes in the auditory periphery apparently linked to the
most basic of stimulus properties become, by the level of
the cortex, part of a much larger neural project of dynamic-
range compression where the effector of the shift in

Figure 1

Gain in action. Mechanisms of auditory gain control operate at multiple levels of the auditory system when an animal is alerted by a novel sound.
Clockwise from bottom right: (A) The anatomy of the outer ear boosts and modifies spectral cues, including those for source location [7]; (B)
membrane responses of cochlear outer hair cells generate longitudinal cellular forces that amplify vibrations of the basilar membrane [10]; (C) rapid
adaptation of responses of midbrain neurons to match of neural output to statistics of the incoming sound [14]; (D) Cortical adaptation in response to
loud sounds preserves sensitivity to quiet sounds — such as the approach of a second tiger [18]; (E) cortical facilitation of STRFs to match incoming
sound frequency/level [20]; (F) medial olivo-cochlear efferents alter rate-versus-sound-level functions to increase output dynamic range for the
representation of discrete signals (tiger) within background (environmental) noise [29].

www.sciencedirect.com Current Opinion in Neurobiology 2009, 19:402–407

406 Sensory systems
response range is not only the underlying statistical distri-
bution of the acoustic cues but, potentially, any environ-
mental cue rendered contextually important by the
conjunction of instantaneous demand, prior experience,
and the receptive-field properties of a given neuron (see
Figure 1).
Gain control and descending systems
Recent anatomical and physiological studies have chal-
lenged the view of ‘bottom-up’ hierarchical processing in
the auditory system, revealing massive reciprocal, des-
cending pathways that stream from all regions of the
auditory cortex to sub-cortical brain structures, by direct
or indirect pathways [27]. Whilst the function of this
corticofugal system remains to be determined, one of
its effects may be gain control. Perhaps the best-charac-
terised descending pathway is the medio-olivocochlear
bundle, or MOC pathway, the efferent input to the
OHCs. It has long been appreciated that MOC stimu-
lation can alter the gain of rate-level functions in the
auditory nerve. Recent studies have extended these
findings, showing complex and variable effects of
MOC stimulation on rate-level functions in both the
ventral cochlear nucleus [28] and the IC [29]. In one of
these studies [29], the authors show a significant effect of
MOC activation in increasing the slope of rate-level
functions of tones played in the presence of background
noise. In addition, in some neurons, MOC activation
resulted in a decrease in tone thresholds. These changes
in threshold and gain render this subset of IC neurons
more able to detect tones in noise and more able to
discriminate between tones of different frequencies.
Clearly, however, any cortical effects on OHCs are likely
to be indirect: investigations by Suga et al. in the bat brain
reveal, amongst many other effects, direct alterations in
gain in the IC as a result of cortical stimulation (reviewed
in [30]).
Interestingly, whilst contemporary research has demurred
from the difficult question of what these efferent-induced
changes might mean for behaviour, half a century ago this
question was actively under scrutiny. Perhaps indeed it is
time to look again at this approach, driven by the work of
Raul Hernandez-Peon, who showed reduced or abolished
evoked potentials in dorsal cochlear nucleus when cats
failed to attend to tones — a gain control phenomenon
the authors ascribed to the descending pathways [31].
One fascinating question concerns the extent to which
complex changes in cortical gain, of the form described
above, impacts on sensory processing in lower brain
centres — it remains to be tested whether responses of
neurons in the IC, for example, are influenced by beha-
viour.
Conclusion
The function of gain control in the auditory system
appears to be one of dynamic-range compression, which
Current Opinion in Neurobiology 2009, 19:402–407
results in improved coding of salient stimuli. Factors
guiding this compression — both stimulus-specific fac-
tors such as the statistical distribution of sound levels, and
behavioural factors such as the difficulty of an auditory
task — are increasingly tractable to investigation. Whilst
it appears that these latter factors are the preserve of
‘higher’ cortical function, the descending auditory path-
way may distribute gain control to more peripheral pro-
cessing sites. It will be fascinating to see how far the
notion of dynamic, context-dependent stimulus encoding
reaches as we discover precisely what constitutes context,
so driving changes in gain, for different parts of the
auditory brain.
References
1. Singh NC, Theunissen FE: Modulation spectra of natural sounds
and ethological theories of auditory processing. J Acoust Soc
Am 2003, 114:3394-3411.
2. Baccus SA: From a whisper to a roar: adaptation to the mean
and variance of naturalistic sounds. Neuron 2006, 51:682-684.
3. Heuer HW, Britten KH: Contrast dependence of response
normalization in area MT of the rhesus macaque. J
Neurophysiol 2002, 88:3398-3408.
4. Pena JL, Konishi M: From postsynaptic potentials to spikes in
the genesis of auditory spatial receptive fields. J Neurosci
2002, 22:5652-5658.
5. Pressnitzer D, Sayles M, Micheyl C, Winter IM: Perceptual
organization of sound begins in the auditory periphery. Curr
Biol 2008, 18:1124-1128.
This study demonstrates that the presumed ‘high-level’ process of
auditory streaming, whereby patterns of tones evolving over time gra-
dually are heard as two independent sound streams can be accounted for
in the responses of neurons in the cochlear nucleus. Neural correlates of
streaming were previously assessed only at the level of the cortex, as it
was assumed that the perceptual attributes of streaming required cortical
contributions.
6. Campbell RA, King AJ, Nodal FR, Schnupp JW, Carlile S,
Doubell TP: Virtual adult ears reveal the roles of acoustical
factors and experience in auditory space map development.
J Neurosci 2008, 28:11557-11570.
7. Hofman PM, Van Riswick JG, Van Opstal AJ: Relearning sound
localization with new ears. Nat Neurosci 1998, 1:417-421.
8. Cooper N: Compression in the peripheral auditory system.
Compression: from Cochlear to Cochlear Implants. New York:
Springer; 2004.
9. Dallos P, Wu X, Cheatham MA, Gao J, Zheng J, Anderson CT,
Jia S, Wang X, Cheng WH, Sengupta S et al.: Prestin-based outer
hair cell motility is necessary for mammalian cochlear
amplification. Neuron 2008, 58:333-339.
10. Ashmore J: Cochlear outer hair cell motility. Physiol Rev 2008,
88:173-210.
11. Dallos P: Cochlear amplification, outer hair cells and prestin.
Curr Opin Neurobiol 2008, 18:370-376.
12. Pienkowski M, Hagerman B: Auditory intensity discrimination as
a function of level-rove and tone duration in normal-hearing
and impaired subjects: the ‘‘mid-level hump’’ revisited. Hear
Res 2009, 253:107-115.
13. Dean I, Harper NS, McAlpine D: Neural population coding of
sound level adapts to stimulus statistics. Nat Neurosci 2005,
8:1684-1689.
This study describes a new means of assessing neural sensitivity to
sound level, suggesting a solution to the ‘dynamic-range problem’ in
hearing. By presenting distributions of sound levels with different ‘high-
probability regions’ these authors demonstrate adaptive coding, with
rate-versus-sound-level functions of midbrain neurons shifting to accom-
modate the current distribution. As a population, neurons are maximally
www.sciencedirect.com
 Gain control mechanisms in the auditory pathway Robinson and McAlpine 407
informative, as judged from Fisher Information, for sound levels just above
the mean level of the distribution.
14. Dean I, Robinson BL, Harper NS, McAlpine D: Rapid neural
adaptation to sound level statistics. J Neurosci 2008,
28:6430-6438.
15. Kvale MN, Schreiner CE: Short-term adaptation of auditory
receptive fields to dynamic stimuli. J Neurophysiol 2004,
91:604-612.
16. Phillips DP, Hall SE: Spike-rate intensity functions of cat
cortical neurons studied with combined tone-noise stimuli. J
Acoust Soc Am 1986, 80:117-187.
17. Rees A, Palmer AR: Rate-intensity functions and their
modification by broadband noise for neurons in the guinea pig
inferior colliculus. J Acoust Soc Am 1988, 83:1488-1498.
18. Watkins PV, Barbour DL: Specialized neuronal adaptation for
preserving input sensitivity. Nat Neurosci 2008, 11:1259-1261.
Employing a similar stimulus paradigm to that of Ref. [13] above, this study
showed that the high proportion of non-monotonic rate-versus-sound-level
functions observed in the auditory cortex had the function of preserving
sensitivity to quiet sounds, even in the context of high sound levels.
19. Fritz J, Shamma S, Elhilali M, Klein D: Rapid task-related
plasticity of spectrotemporal receptive fields in primary
auditory cortex. Nat Neurosci 2003, 6:1216-1223.
20. Fritz J, Elhilali M, Shamma S: Active listening: task-dependent
plasticity of spectrotemporal receptive fields in primary
auditory cortex. Hear Res 2005, 206:159-176.
21. Atiani S, Elhilali M, David SV, Fritz JB, Shamma SA: Task difficulty
and performance induce diverse adaptive patterns in gain and
shape of primary auditory cortical receptive fields. Neuron
2009, 61:467-480.
22. Fritz JB, Elhilali M, Shamma SA: Differential dynamic plasticity of
A1 receptive fields during multiple spectral tasks. J Neurosci
2005, 25:7623-7635.
www.sciencedirect.com
23. Blake DT, Merzenich MM: Changes of AI receptive fields with
sound density. J Neurophysiol 2002, 88:3409-3420.
24. Ulanovsky N, Las L, Nelken I: Processing of low-probability
sounds by cortical neurons. Nat Neurosci 2003, 6:391-398.
This study demonstrates that cortical neurons are sensitive to context in
which relatively simple sounds are heard, evoking stimulus-specific
adaptation (SSA). Such sensitivity of cortical neurons could underlie
the appearance of the mismatch negativity (MMN) response recorded
from human subjects.
25. Ulanovsky N, Las L, Farkas D, Nelken I: Multiple time scales of
adaptation in auditory cortex neurons. J Neurosci 2004,
24:10440-10453.
26. Hui GK, Wong KL, Chavez CM, Leon MI, Robin KM,
Weinberger NM: Conditioned tone control of brain reward
behavior produces highly specific representational gain in the
primary auditory cortex. Neurobiol Learn Mem 2009, 92:27-34.
27. Winer JA, Lee CC: The distributed auditory cortex. Hear Res
2007, 229:3-13.
This article highlights the extensive projections of the auditory cortex,
including to lower brain centres where, presumably, it can exert influ-
ences to the level of the sensory hair cells in the cochlea.
28. Mulders WH, Seluakumaran K, Robertson D: Effects of
centrifugal pathways on responses of cochlear nucleus
neurons to signals in noise. Eur J Neurosci 2008, 27:702-714.
29. Seluakumaran K, Mulders WH, Robertson D: Unmasking effects
of olivocochlear efferent activation on responses of inferior
colliculus neurons. Hear Res 2008, 243:35-46.
30. Suga N, Gao E, Zhang Y, Ma X, Olsen JF: The corticofugal
system for hearing: recent progress. Proc Natl Acad Sci U S A
2000, 97:11807-11814.
31. Hernandez-Peon R, Scherrer H, Jouvet M: Modification of
electric activity in cochlear nucleus during attention in
unanesthetized cats. Science 1956, 123:331-332.
Current Opinion in Neurobiology 2009, 19:402–407