Somatosensory and Motor Research, March–June 2011; 28(1–2): 11–18
Barrels XXIII: Barrels by the shore
Department of Neuroscience, Columbia University, New York, NY, USA and
Department of Psychology,
Queens College, City University of New York, Flushing, NY, USA
(Received 12 January 2010; accepted 12 January 2010)
The 23rd annual Barrels meeting was held on the University of California, San Diego campus and highlighted the latest
advances in the whisker-to-barrel pathway and beyond. The annual meeting brought together investigators from a dozen
countries to present their data in posters and short talks. The meeting focused on several themes, first the barrel system was
used as a model to study the consequences that result from alterations in the normal pattern(s) of development. A second
session focused on what happens to whisker information once it leaves the layer IV barrel. A third session addressed issues of
coding within the barrel system and a final session highlighted the latest advances in the engineering of transgenic mouse
lines. The meeting highlighted the utility of the barrel system to study cortical circuitry in the normal and pathological state.
Keywords: Whisker, vibrissa, barrel, meeting
Forty years after the initial publication of the
discovery of the cortical barrels, the 23rd annual
Barrels meeting convened in the Calit2 Auditorium
on the campus of the University of California, San
Diego on 11 and 12 November 2010. The meeting
welcomed 90 researchers from a dozen countries to
discuss the latest advances in the rodent sensorimo-
tor system (see Appendix 1 for the complete
The opening session focused on how the barrel
system can serve as a model to investigate what can
happen behaviorally, genomically, physiologically,
and anatomically when the system is disrupted by
developmental disorders. Fan Wang (Duke
University, USA) introduced and moderated the
morning session, reminding the audience of the
devastating consequences on neurocognitive devel-
opment in humans that result from Rett syndrome,
Fragile X, and Reelin disorders.
Sacha Nelson (Brandeis University, USA)
focused on the physiological genomics of Rett
syndrome. Rett syndrome is the second most
common genetic cause of mental retardation and is
due to the specific mutation of the MeCp2 gene,
in addition to the neurocognitive sequelae there are
disruptions of the autonomic nervous system as well
as sleep and respiratory abnormalities. He focused on
determining the expression of genes found in specific
cellular phenotypes and how their misregulation
could lead to the disruption of neural circuits
which directly leads to the resultant pathology.
Mice who have had their MeCp2 gene deleted
recapitulate the disease and it was found that cortical
neurons from these animals showed a reduction of
excitatory currents and an increase in inhibitory
currents under spontaneous conditions and display
reduced long-term potentiation and smaller excita-
tory post-synaptic potentials when synaptic inputs
were stimulated. Interestingly, genomic analyses
revealed that cell adhesion molecules that are
important in the formation and maintenance of
synapses were disrupted in the knockout animals.
Andreas Frick (University Bordeaux 2, France)
focused his investigations on the most common
Correspondence: J. C. Brumberg, PhD, Department of Psychology, Queens College, CUNY, Flushing, NY 11568, USA. Tel: þ1 718 997 3541.
Fax: þ1 718 997 3257. E-mail:
ISSN 0899–0220 print/ISSN 1369–1651 online ß 2011 Informa Healthcare Ltd.
DOI: 10.3109/08990220.2011.563602
inherited mental disorder, Fragile X syndrome, using
mouse models where the Fmr1 gene had been
deleted. Behavioral testing showed that knockout
animals were able to complete a gap crossing task
quicker, due to fewer whisks needed to make the
decision to jump, and they were able to cross wider
gaps compared to wild type animals. Voltage-
sensitive dye experiments revealed more excitation
following whisker stimulation in the Fragile X
animals. A hallmark of Fragile X syndrome is
dendritic alterations including increases in spine
density. The FMRP protein (the product of the
Fmr1 gene) targets many dendritic ion channels,
in addition to cytoskeleton proteins, including K
(GIRK3, Kv 3.1, BkCa), Ca
(Cav1.3), and cation
(hyperpolarization activate cation current (HCN))
channels whose misregulation was hypothesized to
impact the neurons’ computational abilities.
Experiments revealed that neurons recorded in
slices from knockout animals had less membrane
‘‘sag’’ in response to hyperpolarizing current pulses,
were more excitable in response to depolarizing
pulses, and showed lower resonance frequencies and
greater ability to summate synaptic inputs due largely
to a decrease in HCN currents. Due to a reduction in
the large conductance Ca
-dependent K
which normally would put the brakes on runaway
excitation, there was increased excitability in the
dendrites of knockout mice. These results confirmed
the hypothesis that the neocortical pyramidal neu-
rons of Fragile X mice have altered computational
abilities which may underlie some of the neurocog-
nitive deficits observed in afflicted individuals.
Jochen Staiger (George-August-Universitat,
Germany) concluded the session describing his
laboratories’ investigations of the reeler mouse. The
audience was reminded that in reeler animals the
cortex develops ‘‘inside out’’ with neurons normally
fated to the deep layers being found closer to the pial
surface and the normally superficial neurons locating
closer to the white mater. Although the ventral
posterior medial nucleus of the thalamus is unaf-
fected in these animals their thalamocortical projec-
tions are more widely distributed throughout the
cortical column and do not aggregate into barrel-like
units. Using in situ hybridization and indicators for
supragranular, granular, and infragranular neurons
it was seen that the thalamocortical afferents still
targeted granular fated neurons even if they were not
located in their normal position within the cortical
The session concluded with the realization that
developmental disorders through their alterations in
neural circuits directly lead to the observed neuro-
cognitive and other pathological phenotypes con-
fronted by clinicians. Only through careful dissection
of the underlying neural circuits will we be able to
understand how these alterations lead to the
observed pathologies and stimulate the development
of therapeutic interventions.
Following a brief coffee break the morning
resumed with a series of short talks moderated by
Arthur Houweling (Erasmus University, the
Netherlands). Leading off, Dudi Deutsch
(Weizmann Institute of Science, Israel) focused on
the variability inherent to rat whisking. Utilizing a
head-fixed preparation with all but three whiskers
clipped (C1, C2, D1) he and his colleagues
monitored free whisking and whisking in the
presence of an object placed in the whisking path.
It was found that whiskers on the same side of the
face were very correlated and less correlated with
whiskers on the opposite side of the face. In general,
the amplitude of the whisking was more variable than
the duration of the whisking cycle. When contacting
an object there was a large increase of amplitude on
the contralateral side with no significant impact on
whisking duration. Detailed analysis of individual
whisks revealed ‘‘pumps’’ wherein periods of nega-
tive velocity were observed during protraction in
25% of all contact whisks. They concluded that there
were separate neural controllers for whisking ampli-
tude and duration. From the same group, Ehud
Ahissar (Weizmann Institute of Science, Israel)
revealed the discovery of Homo rehovotus whiskerus
a graduate student outfitted with whisker-like appen-
dages attached to their fingers as a means of
capturing all the relevant variables in regards to a
sensory–motor task—‘‘whisking’’ and aperture width
discrimination. The synthetic whiskers were outfitted
with motion and force sensors. Increasing accuracy
was correlated with more coordinated movement.
It was found that changes in motor strategies by
themselves directly led to increased perceptual
resolution. The more ‘‘whisking’’ cycles (more
sensory sampling) the smaller differences in aperture
width which could be detected. In general, percep-
tion emerges from a convergence process including
sensory and motor variables. The session concluded
with Jason Ritt (Boston University, USA) arguing
for creating standards for the measurement and
reporting of whisker behaviors and their neural
correlates. The key issue confronting researchers is
how to measure the relevant variables given that little
is known about the mechanics of the vibrissa follicle
and how these variables might influence sensory
transduction. It was pointed out that it is still unclear
as to what behavioral tests should be conducted and
in what reference frame whisker angles should be
referenced. Finally, when using different tracking
strategies to follow whisker movements it was
suggested that estimation errors/assumptions should
be highlighted in the relevant sections of the
12 W. Zhang & J. C. Brumberg
After the annual business meeting (chaired by
Joshua C. Brumberg, Queens College, CUNY,
USA) and a scrumptious lunch, the afternoon
session of short talks began under the direction of
Karel Svoboda (Janelia Farms, USA). The session
was started off by Hiroshi Kawaski (The University
of Tokyo, Japan) who focused on the mechanism that
governs barrel formation. He compared the rate of
barrel formation in control animals vs those from
mothers who were induced to deliver 1 day early.
The size of the resultant litters and their body weights
and their brains’ cortical thickness were unaffected,
but the barrels of the preterm animals developed
earlier. The birthing process results in a decrease in
serotonin levels which accounted for the early barrel
development although the rate of development is the
same as in control animals. Next, Qian-Quan Sun
(University of Wyoming, USA) followed the pro-
gression of the balance of excitatory and inhibitory
(EI) inputs onto neurons throughout the barrel
column. Within the layer 4 barrel the EI ratio
decreased from postnatal day (PND) 8 to PND18
and then remained stable. In the supragranular layers
stable ratios were not obtained until PND30, layer 5
followed a similar developmental timeline to layer 4.
The decrease in the EI ratio was largely accounted
for by increases in inhibitory conductances. Mary
Ann Wilson (Johns Hopkins University, USA)
followed with a presentation on how perinatal
exposure to lead can impact spine development
within the barrel. Nursing mothers were exposed to
lead in their drinking water for the first 10 days of
their pups’ lives which resulted in a smaller overall
barrel field in the pups. Although there were no
changes in the total number of neurons or in their
dendritic architecture there was a decrease in the
branching of the thalamocortical axons and an
increase in spine density. Finally, Rodrigo Kujis
(Encephalogistics, Inc., USA) reminded the audi-
ence of the devastating consequences of Alzheimer’s
disease and the lack of therapeutic interventions.
Although primary sensory cortices had been thought
to be spared during Alzheimer’s disease, recent data
show that this is not the case and that lesions can be
found in the barrel cortex of mouse models of
Alzheimer’s disease suggesting that the barrel cortex
can serve as a model system for studying the
progression of the disease as well as for testing the
efficacy of potential treatments.
The final short talk session of the day was led by
Qian-Quan Sun (University of Wyoming, USA).
Starting off was Lu Li (Helen Wills Neuroscience
Institute, USA) who looked at rapid plasticity in the
barrel cortex using whole cell in vivo recordings. The
presentation highlighted two types of plasticity and
their distinct mechanisms; hebbian plasticity which
requires positive feedback vs homeostatic plasticity
which requires negative feedback. To probe for these
two types of plasticity in the barrel cortex, D row
whiskers were trimmed for 1–10 days starting at
PND20 and recordings were obtained in vivo from
supragranular neurons under urethane anesthesia. It
was found that there was a decrease in local field
potentials following 3, 5, or 10 days of deprivation
and following 3 days of deprivation there was an
increase in the magnitude of the long latency
response whereas after 5 days there was a decrease
in the overall number of action potentials in response
to principal whisker deflections. Whole cell record-
ings revealed that deprivation decreased overall
synaptic conductance with inhibitory conductances
decreasing more than excitatory which was consis-
tent with a model of rapid homeostatic plasticity
resulting from short-term deprivation in the supra-
granular layers. Craig Brown (University of
Victoria, Canada) focused on the role 4 nicotinic
receptors had on experience-driven cortical depres-
sion in the mouse somatosensory cortex using in vivo
voltage-sensitive dye imaging. The C1 whisker was
trimmed and then imaging commenced either 3, 7,
or 21 days post-trimming. It was found that after 3 or
7 days post-trimming there was a decrease in the
voltage-sensitive dye response to C1 deflections
which returned to normal by 21 days post-trimming.
It was determined that there was an increase in the
4 nicotinic receptor post-trimming which was
colocalized with the post-synaptic scaffolding protein
PSD95 and most GABAergic neurons had 4 puncta
in apposition to their somata. Application of 4
agonists depressed responses and if following trim-
ming 4 antagonists were continuously applied to the
barrel cortex via an osmotic pump the trimming-
induced depression was blocked. In sum, these
results suggest that 4 receptors on GABAergic
interneurons account for the majority of the trim-
ming-induced depression in the voltage-sensitive dye
response. The day ended with a stimulating poster
session and then a barbecue dinner listening to the
waves breaking on the shoreline in La Jolla, CA.
The second day of the conference opened with
a session focused on understanding the barrel cortex
as a part of a larger sensorimotor neural network.
Specifically, the question was posed, how is periph-
eral sensory information conveyed and propagated
beyond the layer IV barrel? David Kleinfeld
(University of California, San Diego, USA) intro-
duced and moderated this session, reminding the
audience that instead of an isolated computational
unit, the barrel cortex is strongly interconnected with
the nearby primary motor cortex (M1) as well as the
secondary somatosensory cortex (S2).
Carl Peterson (EPFL, Switzerland) focused on
how intrinsic brain states can modulate the whisker-
evoked responses of barrel cortex neurons in awake,
Barrels XXIII: Barrels by the shore 13
behaving mice. Voltage-sensitive dye (VSD) imaging
showed that cortical voltage responses of a passive
whisker stimulus were dramatically impacted by the
behavioral state of the animal. In awake and
quiescent animals, whisker stimulation elicited large
depolarizations in the barrel cortex that spread
almost immediately (30 ms post-stimulus) into both
M1 and S2. In contrast, in animals that were actively
whisking, passive stimulus elicited only small depo-
larizations that remained localized to the barrel
cortex. The VSD imaging results were confirmed
by intracellular patch-clamp recordings from layer
2/3 (L2/3) neurons. Peterson then investigated the
responses of cortical neurons to active-touch, or
object-contact during active whisking, using intra-
cellular patch-clamp recording. Recordings form
cortical neurons when rats where engaged in active-
touch elicited mixed excitatory and inhibitory con-
ductances which showed a large degree of variability
and action-potential firing was unreliable. However,
contact of object during active-touch increased the
correlation of sub-threshold Vm between neighbor-
ing cells. The second part of the talk focused on the
response of cortical neurons during a detection task.
Mice were trained to detect a magnetic deflection of
a single whisker for water rewards. Peterson showed
that the voltage responses of cortical L2/3 neurons
were highly dependent on the pre-stimulus EEG
state of the animal. Specifically, when the EEG is in a
slow-oscillatory state, the neurons show large stimu-
lus-elicited depolarization in Vm and when the EEG
is in a desynchronized state, neurons show very little
Vm responses. The performance of the animal was
only weakly correlated with the pre-stimulus brain
state, where the miss trials showed slightly higher
power in the low-frequency (1–5 Hz) oscillations.
Ron Frostig (University of California Irvine,
USA) focused his investigation on using the spread
of activity in barrel cortex as a general model for
mammalian sensorimotor cortex activation. He first
showed, using intrinsic imaging as well as extra-
cellular recording, that the cortical area activated by a
single-whisker periodic stimulus is about 15 mm
, far
larger than the area of a single barrel column (0.5
). The spread of cortical activation is radially
symmetrical, even when the center is near a border
between different sensory areas (e.g., S1 and primary
auditory cortex (A1)). To investigate the anatomical
basis for this spread of excitation, a tracer was
injected into L2/3 of individual barrels, and axons
local to the injection site were labeled and were
shown to radially spread several millimeters from the
center. To further study the underlying mechanism
of this non-specific local spread of excitation, Frostig
performed a series of experiments where the gray
matter between an array of eight extracellular
electrodes was transected. Local field potential
(LFP) signals in distant electrodes disappeared after
transection, demonstrating that the spread of activa-
tion is mediated by intracortical connections. Tracer
labeling was also attenuated by the transection.
Additional support for the large symmetrical spread
came from his study of cortical infarcts induced by
permanent occlusion of the middle cerebral artery
(pMCAO). When a single whisker was stimulated
immediately or 1 h after pMCAO, the cortex was
completely protected from the stroke. If whisker
stimulation commenced 2 h after pMCAO, 80% of
the animals showed complete cortical protection.
However, when a single whisker was stimulated 3 h
after pMCAO, the resulting infarct was larger than
what would have been obtained without stimulation,
and the resultant infarct matches the typical volume
of cortical activation evoked by a single whisker.
Imaging results similar to the ones obtained by
Frostig have been shown in other sensory cortical
areas such as A1 and V1 using either VSD or
intrinsic imaging. The anatomical results have also
been demonstrated in other regions of the sensor-
imotor cortex. Frostig therefore suggested that in
response to a point sensory stimulus, a large,
symmetrical sub-threshold spread of activation is a
fundamental motif of mammalian sensorimotor
The session concluded with Tim Murphy
(University of British Columbia, Canada) discussing
his laboratory’s investigation of widespread patterns
of cortical activation under different conditions.
Using VSD imaging, he found that spontaneous
oscillation in Vm take the form of traveling waves in
both anesthetized and awake mice. The traveling
waves are highly synchronous between hemispheres
and correspond to increases in the power of the low-
frequency EEG. Areas along the midline typically
initiate the traveling cortical depolarization, and are
termed the ‘‘core of spontaneous activity’’. Recent
sensory experiences can affect the pattern of sponta-
neous activity by initiating the traveling wave near the
area recently activated by the sensory stimuli.
Activation motifs found during spontaneous travel-
ing waves were found to resemble the patterns of
activity generated by sensory stimuli. Interestingly,
sensory training stimuli can increase the amount of
match between spontaneous motifs and evoked
patterns of activity. Lastly, Murphy showed that, in
transgenic animals whose cortical layer 5b neurons
express channelrhodopsin (ChR), sensory stimuli-
evoked patterns of activity can be mimicked by local
light activation in the corresponding sensory cortical
The session concluded with the realization that the
community must start viewing the barrel cortex as an
integral part of a larger sensorimotor cortical net-
work. Not only are there specific long-range
14 W. Zhang & J. C. Brumberg
reciprocal connections between barrel cortex and
motor cortex (as well as other higher sensory areas),
but there are also non-specific local connections
between primary sensory cortices of different mod-
alities. Only when carefully considering these short-
and long-range intracortical connections can the
ultimate role of the barrel cortex in performing
cortical computations be truly understood.
Following a brief coffee break the morning
resumed with a talk by Hongkui Zeng (Allen
Institute of Brain Sciences, USA) on the latest
advances in the engineering of transgenic mouse
lines. The speaker first reminded the audience of the
importance of transgenic technologies as tools to
dissect the function of specific cell types in complex
circuits. The Allen Institute has created a cell-type
selective mouse genetic toolkit system to facilitate the
study of neural circuits. The toolkit system includes
the generation of Cre-driver lines that target specific
cortical cell types, Cre-responder lines with strong
expression of fluorescent probes for neuronal tracing,
calcium imaging (gCAMP3), and membrane pro-
teins for photostimulation (Channelrhodopsin,
Halorhopsin, and Arch). A set of corresponding
AAV viral vectors will also be soon available, which
can be used in conjunction with the transgenic mice.
Experiments validating the functionality of these
probes are still ongoing, but preliminary results
suggest that investigators may soon be able to
purchase lines of mice to study specific efferent and
afferent pathways using optical means. Zeng also
described the Mouse Brain Connectivity Atlas
project, the aim of which is to create a whole-brain,
mid-to-high-resolution, three-dimensional map of
axonal projections in the mouse brain. The atlas
will be created primarily using genetic tracing
approaches that utilize a variety of cell-type specific
Cre lines and Cre-dependent viral tracers. Both the
raw data as well as the 3-D models will be presented
on a public online database to create 2-D and 3-D
searchable interactive tools and is hoped to be
completed by the end of 2012.
The morning session concluded with a quick data
blitz session moderated by Randy Bruno
(Columbia University, USA). Joshua C.
Brumberg (Queens College, CUNY, USA) pre-
sented a recent study investigating the physiological
properties of two types of corticothalamic (CT)
neurons: (1) the CT-VPM neurons and (2) the
CT-POM neurons. CT neurons are identified by
injections of retrograde tracers into either VPM or
POM. CT-VPM neurons are typically located in L6
of barrel cortex while CT-POM neurons are found
in L5b. Based on action potential (AP) half-width
measured by patch-clamp recordings of retrogradely
labeled neurons in thalamocortical slices, CT-VPM
neurons have broader APs compared to CT-POM
neurons. Both cell types receive thalamic inputs.
In response to a pair of thalamic stimulations, CT-
POM neurons showed response facilitation while
CT-VPM neurons showed neither facilitation nor
depression. Similarly, in response to a train of eight
pulses, CT-POM neurons continued to show
response facilitation, and CT-VPM neurons
showed clear response depression. Vincent Jacob
(Cardiff University, Wales) finished the data blitz
session by showing sensory deprivation can differen-
tially affect subtypes of pyramidal neurons in L5 of
barrel cortex. After single-row whisker deprivation
for 10 days in 6-week-old rats, responses to spared
whisker potentiated in L5 regular spiking (RS)
neurons but not in L5 intrinsically bursting (IB)
After lunch, the afternoon session started with a
series of short talks moderated by Jason Ritt (Boston
University, USA). The series started off with Gaute
T. Einevoll (Norwegian University of Life Sciences,
Norway) who created a thalamocortical network
model of the barrel column using population firing
data. Multi-unit activity (MUA) and local field
potential (LFP) data were recorded with laminar
electrodes in the barrel cortex, and MUA recordings
were obtained with a single electrode in the
thalamus. Responses of both thalamic and cortical
neurons to a single-whisker stimulus with varying
velocity and amplitude were recorded. Firing rates
extracted from MUA recordings were in turn used to
identify population firing-rate models. He found that
the thalamus to L4 connection was best fitted by a
model with fast feed forward excitation from VPM
combined with a slower inhibitory process due to
feed forward and/or recurrent connections. The
model predicted that the thalamocortical circuit is
optimally stimulated by rapid changes in the thalamic
firing rate. Information transfer within the cortical
column, on the other hand, was better fitted with
a simple feed forward population firing-rate model
combined with linear or mixed linear–parabolic
activation function, which predicts that the intracor-
tical circuits are low-pass filters that respond best to
slow-varying inputs from cortical L4 neurons. Next
Robert Sachdev (Yale University, USA) discussed
the VSD response evoked in mouse barrel cortex by
single-whisker stimuli. He showed that in urethane
anesthetized mice, single-whisker stimulus elicits a
wave of depolarization. A longer whisker stimulus
caused a slower rise in the VSD signal and a
persistent depolarization because the on-response is
blending with the off-response. The persistent
depolarization cannot be mimicked by a pair of
whisker stimuli. Paired whisker stimuli at short
intervals (8 ms) do not generate a second response
but only evoke a larger spread of the initial cortical
depolarization. At longer intervals (100–200 ms), the
Barrels XXIII: Barrels by the shore 15
second stimuli produced a VSD response that is
slower to rise and slower to decay, but do not spread
as far as the initial response. Lastly, the extent of the
area of activation observed by VSD imaging is not
dependent on direction of the whisker stimuli.
Finally, Alison L. Barth (Carnegie Mellon
University, USA) presented the work of her labora-
tory developing an unbiased method to assess the
firing activity of individual neurons in the barrel
cortex. They used a fos-GFP transgenic mouse to
examine the properties of cells with a recent history
of elevated activity. Intriguingly, their investigation
has shown that neuronal responses are extremely
heterogeneous in vivo. In barrel cortex, only layer 4
neurons and a very small proportion of layer 2/3
neurons show Fos-promoted GFP expression in
response to sensory stimulation. In vitro patch-
clamp recording of fos-GFP-positive neurons were
not intrinsically more excitable than other neurons,
but receive more synaptic inputs and are highly
interconnected. She then performed dual in vivo
targeted cell-attached recording, and demonstrated
that fos-GFP-positive neurons spontaneously fire
more and earlier than fos-GFP-negative neurons.
Fos-GFP-positive neurons are also more likely to fire
in bursts. Lastly, whisker-trimming did not affect the
proportion of fos-GFP-positive neurons within the
The final session of the day focused on encoding
and decoding of sensory inputs in the whisker–barrel
system and other primary sensory cortical areas.
David Golomb (Ben Gurion University, Israel)
introduced the session by reminding the audience of
the difficulties of interpreting sensory-stimulus-
evoked physiological data, and the existing debates
over the basis of cortical neural coding.
Garrett Stanley (Georgia Institute of
Technology, USA) started off the session by discuss-
ing how adaptation affects thalamocortical transfor-
mations of peripheral somatosensory information.
Using simultaneous single-unit recordings in the
VPM and the barrel cortex in anesthetized rats, they
discovered that adaptation differentially influences
the thalamus and cortex. In response to repeated
whisker stimuli (12 Hz) of various velocities, L4
cortical neurons adapt strongly in response ampli-
tude. Adaptation in turn increases the slope of the
velocity–sensitivity curve (angular velocity vs number
of APs in 30 ms window) of cortical neurons, making
it easier to discriminate different stimulus velocities
based on firing rate alone. VPM neurons, on the
other hand, were shown to adapt to repeated stimuli,
but less than cortical neurons. While the velocity–
sensitivity curve of VPM neurons does not change in
the adapted state, there is a significant decrease
in synchrony between VPM neurons. This decrease
in synchrony could account for the change in the
slope of the velocity–sensitivity curve of cortical L4
neurons. The second part of the talk involved his
more recent work involving observer analysis of VSD
imaging of cortex and anesthetized rats. In other
words, if an ideal observer was present could they
determine the nature of the sensory input based on
the observed VSD signal. The area of activation
detected by VSD imaging increases with whisker
stimulus velocity, therefore, for an ideal observer to
discriminate between stimulation of two neighboring
whiskers, there is an optimal stimulus velocity which
would still generate significant VSD signal but also
minimal amount of spread outside of the stimulated
barrel allowing for discrimination.
Next, Brent Dorion (University of Pittsburgh,
USA) presented several strategies by which a
neuronal network could be used to change output
correlations when there is shared input correlation.
Using a model of a network of neurons sharing a
common input source, and several non-shared noise
sources, he demonstrated that the background noise
level of a neuron can change the firing-rate gain
control of the cell, which in turn changes the output
noise correlation of the neurons. He further showed
that with high background noise, the output correla-
tion of the network showed higher synchrony with
a shorter window of analysis (3 ms) but lower
synchrony with longer window of analysis (over 10
ms). In vitro recording from pairs of cortical L2/3
neurons while injecting different levels of noisy
conductances using a dynamic clamp confirmed
this finding. A second strategy is the recruitment of
feed forward inhibitory circuits with higher input
amplitudes, which could create a negative image of
the input signal, which in turn decreases the amount
of output synchrony of the principal neurons. Dorion
further demonstrated that this strategy has been
utilized by the electrosensory system of the weakly
electric fish.
The meeting was concluded with a talk by Ken
Harris (Imperial College London, UK) focused on
the sensory-evoked population response of auditory
corticalneurons. Using extracellular multi-unit
recordings (MUA) from A1 of rats, he found that
the population responses of A1 neurons to a single
tune resembled spontaneous up-like events which
occur in the absence of sensory stimuli. Both
spontaneous and evoked events exhibited sparse,
spatially localized activity in L2/3 pyramidal neurons,
and densely distributed activity in larger L5 pyrami-
dal neurons and putative interneurons. The only
difference between spontaneous and evoked events
was their laminar propagation: spontaneous events
initiated in the deep layers and propagated upward
while evoked activity initiated in the thalamo-
recipient layers and then propagated throughout the
column. In both un-anesthetized and urethanized
16 W. Zhang & J. C. Brumberg
rats, global activity fluctuated between a ‘‘desyn-
chronized’’ state characterized by a low-amplitude,
high-frequency LFP and a ‘‘synchronized’’ state of
larger, lower frequency waves. Computational stu-
dies done in his lab suggested that cortical neuronal
responses could be modeled by a simple dynamical
system model fitted to the spontaneous activity
immediately preceding stimulus presentation. This
result reflected a nonlinear self-exciting system in
synchronized states and an approximately linear
system in desynchronized states.
After 2 days of stimulating talks, posters, and
discussions the 23rd annual Barrels meeting drew to
a close with a commitment to reconvene in a year’s
time in Baltimore, MD. The meeting once again
confirmed the utility of the barrel system as a model
to study not only cortical development and function-
ing, but also as a model to study neuropathology and
developmental disorders.
The Barrels organizing committee (Joshua C.
Brumberg (Chair), Randy Bruno, Mitra Hartmann,
David Kleinfeld, Jochen Staiger, and Mary Ann
Wilson) would like to thank Nancy Steinmetz and
Kathy Diekmann for their invaluable help.
Declaration of interest: The authors report no
conflicts of interest. The authors alone are respon-
sible for the content and writing of the paper.
Appendix 1. Barrels XXIII schedule
Thursday, 11 November
9:00–9:05 Welcome Joshua C. Brumberg, Queens College, CUNY
Introduction to local area David Kleinfeld, UCSD
9:05–11:15 Development Gone Haywire
9:05–9:15 Introduction/overview Fan Wang, Duke University
9:15–9:45 Sacha Nelson, Brandeis University, USA
Physiological genomics of Rett syndrome
9:45–10:15 Andreas Frick, University Bordeaux 2, France
Pathophysiology of information processing in neocortical circuits in Fragile X syndrome
10:15–10:45 Jochen Staiger, Georg-August-Universita
t, Go
ttingen, Germany
Remodeling of (thalamo-)cortical circuits in reeler mice showing severe neuronal migration defects
10:45–11:15 Discussion
11:15–11:45 Coffee Break
11:45–12:45 Short Platform Talks 1
Moderator: Arthur Houweling, Erasmus MC, the Netherlands
11:45–12:00 D. Deutsch
, M. Pietr
, P. M. Knutsen
, E. Ahissar
and E. Schneidman
Weizmann Institute of Science, Rehovot, Israel,
University of California, San Diego, USA
Closed loop whisking: effects of contacts
12:00–12:15 Avraham Saig
, Amos Arieli and Ehud Ahissar
Weizmann Institute of Science, Rehovot, Israel
Improving perceptual accuracy via motor and not sensory modifications
12:15–12:30 Jason Ritt
, Jason Wolfe
, Mitra Hartmann
, Ehud Ahissar
, Michael Brecht
and Christiaan de Kock
Boston University,
Humboldt University, Berlin,
Northwestern University,
Weizmann Institute of Science,
VU University,
Establishing community standards for measurement and reporting of whisker behaviors and their neural correlates
12:30–12:45 Discussion
12:45–12:50 Business Meeting (Joshua C. Brumberg, Queens College, CUNY)
12:50–2:30 Lunch Break
2:30–3:45 Short Platform Talks 2
Moderator: Karel Svoboda, Janelia Farms
2:30–2:45 Tomohisa Toda, Itaru Hayakawa and Hiroshi Kawasaki
The University of Tokyo, Japan
The role of birth in somatosensory map formation in the mouse barrel cortex
2:45–3:00 Z. Zhang
and Q.-Q. Sun
University of Wyoming
A direct measure of E/I balance across different layers of somatosensory cortex during postnatal development
3:00–3:15 Mehdi Pedramfard, Manek S. Aulakh, Jong J. Park, Patrice D. Carr, Michael V. Johnston, Mary E. Blue and Mary Ann
Johns Hopkins University School of Medicine
Effect of lead exposure on dendritic spine development in rodent barrel cortex
3:15–3:30 Rodrigo O. Kujis
Encephalogistics, Inc.
The barrel cortex as a novel assay for selective vulnerability and sparing in Alzheimer’s disease
(continued )
Barrels XXIII: Barrels by the shore 17
3:30–3:45 Discussion
3:45–4:00 Coffee Break
4:00–5:00 Short Platform Talks 3
Moderator: Qian-Quan Sun, University of Wyoming
4:00–4:15 Lu Li
and Daniel E. Feldman
Helen Wills Neuroscience Institute
A novel and rapid component of whisker response plasticity in rat somatosensory (S1) barrel cortex
4:15–4:30 Craig E. Brown
, Dani Sweetnam, Maddie Beange, Thomas Watson and Raad Nashmi
University of Victoria
A role for 4
nicotinic receptors in experience-driven cortical depression in adult mouse somatosensory cortex in vivo
4:30–4:45 Peter W. Hickmott
and Hubert Dinse
University of California, Riverside,
Ruhr University Bochum, Germany
Characteristics of thalamocortical EPSCs and IPSCs in hindpaw S1 in adult and aged rats in vitro
4:45–5:00 Discussion
5:00–5:30 Break
5:30 Poster Session
7:00 Dinner
Friday 12 November
9:00–11:00 Beyond the Barrel
9:00–9:10 Introduction/overview David Kleinfeld, UCSD
9:10–9:40 Carl Peterson, EPFL, Switzerland
Cortical sensorimotor integration
9:40–10:10 Ron Frostig, University of California Irvine
Activity spread beyond the barrel as a general model for mammalian sensory–motor cortex activation
10:10–10:40 Tim Murphy, University of British Columbia, Canada
Imaging widespread consensus patterns within spontaneous and sensory-evoked cortical depolarization in vivo,
implications for normal function and recovery after injury
10:40–11:00 Discussion
11:00–11:15 Coffee Break
11:15–12:00 Emerging Techniques
11:15–11:30 Hongkui Zeng, Allen Institute for Brain Sciences, USA
Mouse genetic toolkit for probing neural circuits and mapping connectivity
11:30–11:45 Discussion
11:45–12:30 Data Blitz
Moderator: Randy Bruno, Columbia University
12:30–2:00 Lunch
2:00–3:00 Short Platform Talks 4
Moderator: Jason Ritt, Boston University
2:00–2:15 Gaute T. Einevoll
, Patrick Blomquist
, Anna Devor
, Ulf G. Indahl
, Istvan Ulbert
and Anders M. Dale
Norwegian University of Life Sciences, Norway,
Massachusetts General Hospital,
University of California, San Diego,
Hungarian Academy of Sciences, Budapest, Hungary
Estimation of thalamocortical and intracortical network models for the rat barrel system from multielectrode recordings
2:15–2:30 Robert Sachdev
, Douglas Davis
and Vincent Pleribone
Yale University School of Medicine,
The John B. Pierce Laboratory
Traveling waves evoked in mouse barrel cortex by single whisker stimuli
2:30–2:45 L. Yassin
, B. L. Benedetti, J.-S. Jouhanneau, J. Wen, J. F. A. Poulet and A. L. Barth
Carnegie Mellon University
Unbiased methods to assess the firing activity of individual neurons in the neocortex have revealed that a large proportion
of cells fire at extremely low rates
2:45–3:00 Discussion
3:00–3:15 Coffee Break
3:15–5:15 Encoding and Decoding Sensory Inputs
3:15–3:25 Introduction/overview David Golomb, Ben Gurion University
3:25–3:55 Garrett Stanley Georgia Institute of Technology
Decoding the thalamocortical circuit
3:55–4:25 Brent Dorion University of Pittsburgh
Long-term plasticity and sensory response modulation
4:25–4:55 Ken Harris Imperial College London
How do neurons work together? The view from auditory cortex
4:55–5:15 Discussion
5:15 Adjourn
* indicates who is giving the presentation.
18 W. Zhang & J. C. Brumberg
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