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The Journal of Neuroscience, November 15, 2002, 22(22):9651-9655
BRIEF COMMUNICATION
Role of Thalamocortical Sensory Suppression during Arousal:
Focusing Sensory Inputs in Neocortex
Manuel A.
Castro-Alamancos
Department of Neurology and Neurosurgery, Montreal Neurological
Institute, McGill University, Montreal, Quebec H3A 2B4,
Canada
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ABSTRACT |
The thalamus serves as a gate that regulates the flow of sensory
inputs to the neocortex, and this gate is controlled by neuromodulators from the brainstem reticular formation that are released during arousal. We found recently that sensory-evoked responses are suppressed in the neocortex during arousal. This sensory suppression results from
the activity-dependent depression of the thalamocortical connection
caused by increased tonic firing of thalamocortical cells during
arousal. In the present study, the functional consequences of
thalamocortical suppression during arousal were investigated using the
vibrissae system of rodents. The results show that thalamocortical suppression is associated with a strong reduction in the spread of
sensory inputs through the cortex, thus reducing the size of sensory
representations. In addition, when the responses of single cells to
principal and adjacent whiskers are compared, the response to the
adjacent whiskers was found to be strongly suppressed, much more so
than that of principal whiskers. Consequently, the receptive fields of
cortical neurons become more focused to the principal whisker. The
results indicate that thalamocortical suppression during arousal serves
to focus sensory inputs to their appropriate representations in
neocortex, which may be computationally helpful for the spatial
processing of sensory information.
Key words:
receptive field; whisker; barrel cortex; synaptic
depression; sensory processing; behavioral state
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INTRODUCTION |
During arousal states typical of
information processing, electroencephalographic activity is
characterized by low-amplitude fast activity, called activation,
which contrasts with the large-amplitude regular and slow activity
typical of quiescent states (Moruzzi and Magoun, 1949 ). Activation is
produced by the release of several neuromodulators in the thalamus and
cortex. For instance, during arousal, cells in the brainstem
laterodorsal tegmentum increase their firing rates (Steriade et al.,
1990), releasing acetylcholine in the thalamus (Williams et al., 1994),
which depolarizes thalamocortical neurons (McCormick, 1992), increasing
their spontaneous firing rates in the tonic firing mode and enhancing
the transmission of low-frequency sensory inputs through the thalamus
(Steriade, 1969; Singer, 1977; Steriade et al., 1997; Sherman and
Guillery, 2001). The postsynaptic depolarization of thalamocortical
neurons during arousal also strongly facilitates the transmission of
high-frequency sensory inputs through the thalamus (Castro-Alamancos,
2002a,b), which are normally filtered during quiescent states. In
addition, the increased firing rate of thalamocortical neurons during
arousal leads to the activity-dependent depression of thalamocortical synapses producing thalamocortical sensory suppression
(Castro-Alamancos and Oldford, 2002). Thus, during aroused states,
there is an increase in the efficacy of sensory transmission through
the thalamus, especially for high-frequency inputs and, because
of the increased firing of thalamocortical cells sensory inputs
reaching the neocortex during arousal, encounter a depressed
thalamocortical synapse, which causes cortical sensory suppression. The
aim of the present study is to investigate some of the functional
consequences of cortical sensory suppression during arousal.
During anesthesia or quiescent states, sensory inputs spread through
large areas of neocortex, giving rise to large receptive fields and
sensory representations (Armstrong-James and Fox, 1987; Armstrong-James
et al., 1991; Chen-Bee and Frostig, 1996; Moore and Nelson, 1998; Sheth
et al., 1998; Ghazanfar et al., 2000; Petersen and Diamond, 2000;
Brett-Green et al., 2001). These observations suggest that, during
quiescent states, the neocortex favors the spread of activity. Other
studies also in the barrel cortex of rodents have found instead a great
spatial contrast between adjacent whiskers in the barrel cortex (Simons
and Carvell, 1989; Goldreich et al., 1999), primarily mediated by
locally recurrent inhibition (Simons, 1995). The more restricted
receptive fields and barrel independence found by these studies has
been attributed to the use of different anesthetics (Simons et al.,
1992), which produce different levels of brain activation. Thus,
receptive fields and cortical representations may differ between
different levels of arousal. The present study investigated the effect
of brain activation caused by stimulating the brainstem reticular
formation on the responses of cortical neurons to whisker stimulation.
The hypothesis is that thalamocortical sensory suppression during
arousal serves to focus sensory inputs in neocortex (Castro-Alamancos
and Oldford, 2002). Sensory representations and receptive fields in the
barrel cortex of rodents were compared in anesthetized rats between
quiescent states and activated states produced by stimulating the
brainstem reticular formation.
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MATERIALS AND METHODS |
Surgical procedures. Adult Sprague Dawley rats (300 gm) were anesthetized with urethane (1.5 gm/kg, i.p.) and placed in a stereotaxic frame. All skin incisions and frame contacts with the skin were injected with lidocaine (2%). A unilateral craniotomy extended over a large area of the parietal cortex. Small incisions were
made in the dura as necessary, and the cortical surface was covered
with artificial CSF (ACSF) containing the following (in mM): 126 NaCl, 3 KCl, 1.25 NaH2PO4, 26 NaHCO3, 1.3 MgSO4 7H2O, 10 dextrose,
and 2.5 CaCl2 2H2O. Body
temperature was automatically maintained constant with a heating pad.
The level of anesthesia was monitored with field recordings and
limb-withdrawal reflexes and kept constant at approximately stage III/3
using supplemental doses of urethane (Friedberg et al., 1999). At the
end of the experiments, the animals were killed with an overdose of
sodium pentobarbitone (intraperitoneally). The Animal Care Committee of
McGill University approved protocols for all experiments.
Electrophysiological procedures. Extracellular recordings
were performed using electrodes (5-10 M ) filled with ACSF; single units and field potentials were recorded simultaneously via the same
electrodes located in the primary somatosensory neocortex (barrel
cortex) at a depth between 400 and 900 µm (i.e., layers IV-III). These high-impedance electrodes recorded an isolated single neuron. The exact location of the recorded cells was not determined using histological procedures. Coordinates (Paxinos and
Watson, 1982) for the stimulating electrode in the laterodorsal tegmentum (brainstem reticular formation; 100 Hz, 1-sec) were as
follows (in mm, from bregma and the dura): posterior, 9; lateral, 0.7;
depth, 5-6. Electrical stimuli consisted of 200 µsec pulses of <200
µA and were evoked using a concentric stimulating electrode (200-µm-diameter ultra-small concentric bipolar electrode; Frederick Haer Co., Bowdoinham, ME).
Sensory stimulation. The sensory stimulation consisted of
deflecting single whiskers. Two stimulators were used that allowed independently stimulating two whiskers: the principal whisker and an
adjacent whisker. The principal whisker was defined as the one
producing the strongest response for the recorded single neuron. This
was determined by using a hand-held probe to map the individual
responses. The adjacent whisker was one that also discharged the
recorded neuron. The selected whiskers were inserted into stimulators
consisting of glass micropipettes (1-mm-diameter) glued to the membrane
of a miniature speaker. During the experiment, stimulation to each
whisker alternated at 4-12 sec intervals. Application of a 1 msec
square current pulse to the speaker deflected the micropipette and the
whisker inside ~400 µm. The whisker-evoked response was measured
between 5 and 15 msec after the whisker stimulus. Whisker stimulation
was applied between 0.5 and 10 sec after the brainstem reticular
formation stimulation.
Analysis of horizontal spread. A 16 channel linear silicon
probe with 100 µm site spacing (~50-µm-diameter; Center for
Neural Communication Technology, University of Michigan, Ann Arbor,
MI) was placed in layers IV-III of the barrel cortex parallel
to the pial surface. This required inserting the silicon probe with a 315° angle (in the coronal plane) at 3.5 mm lateral from the midline. The probe was advanced ~3 mm from the pia and thus placed
horizontally in layers IV-III. In several animals (n = 2), the location of the probe along layers IV-III was confirmed by
preparing coronal slices in ACSF using standard brain slicing
procedures (Castro-Alamancos, 2002b). This allowed visualizing in a
microscope the tract of the probe penetration. In both cases, the
recording sites of the probe were estimated to be between 650 and 850 µm from the surface. No histological procedure was used. Field
potential recordings were obtained simultaneously from the 16 sites on
the probe in response to deflections of a single whisker. To equalize
the impedance in each site on the probe (~500 K), they were
oxidized before use (Castro-Alamancos, 2000).
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RESULTS |
Thalamocortical suppression during activated states may serve to
focus sensory inputs to their specific cortical representations by
limiting the spread of activity. This was tested by monitoring the
cortical responses along a horizontal strip (1.6 mm) of the barrel
cortex along layers IV-III with 100 µm resolution using a 16 channel
silicon probe (Fig.
1A). Examples of the
field potential responses recorded with this method have been published
previously (Castro-Alamancos and Oldford, 2002). Deflecting a single
whisker produces responses in a large portion of barrel cortex that
exceeds the area of a single cortical barrel (Petersen and Diamond,
2000; Brett-Green et al., 2001). In fact, the extent of the cortex
responding to stimulation of a single whisker was larger than the
extent of the 1.6 mm probe. The activity in neocortex spreads
horizontally through barrel cortex as reflected by the longer
latencies of the responses recorded surrounding the short-latency and
large-amplitude response in the center (Fig. 1B).
However, activation induced by brainstem reticular formation
stimulation strongly limited the size of the neocortical area
responding to a single whisker (Fig. 1B). During
activation, stimulation of a single whisker produced a response in the
neocortex that showed little spread to adjacent territory. As a
consequence, during activated states, the cortical response to
stimulation of single whiskers was focused to a significantly smaller
area. Based on several rats (n = 4), the relative
spread of activity from the center of the representation (i.e., the
recording site on the probe with the shortest latency response; ~5.5
msec) was reduced by 59.5 ± 3% (p > 0.0001; t test) during activation caused by stimulating the
brainstem reticular formation. This relative measure underestimates the
amount of reduction in spread caused by activation because the complete extent of the spread was usually larger than the probe.
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Figure 1.
Sensory representations in neocortex are focused
during activation. A, Schematic representation of the
location of the 16 channel silicon probe placed at a 135° angle in
the barrel cortex to record field potential responses through an
extension of layers IV-III of the barrel neocortex. B,
Contour plot of the amplitude of the negative field potential recorded
from 16 sites (100 µm intervals) along layers IV-III of the barrel
cortex in response to stimulation of a single whisker. Note the spread
of activity under control conditions and the suppression of spread and
focusing of the representation after brainstem reticular formation
stimulation (RF Stim.).
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Because the spread of activity through the cortex is focused
considerably during activation, this should also be manifested in the
focusing of the receptive fields in cortical cells from layers IV-III.
To test this hypothesis, single-unit recordings were obtained from
cells in layers IV-III of the barrel cortex (n = 23 cells). No effort was made to distinguish between these two layers in
the present study. Stimulation of the brainstem reticular formation
resulted in either an enhancement or reduction of the spontaneous
firing rate of the cortical neurons recorded, but, as shown previously,
they all reduced their response to the sensory stimulus
(Castro-Alamancos and Oldford, 2002). The mean spontaneous firing rate
of all of the recorded cells was 3.2 ± 0.5 Hz during control
conditions and 6.1 ± 1 Hz during activation. From this population
of cells, 34% (n = 8 of 23) enhanced their firing
rate, whereas 66% (n = 16 of 23) reduced their firing
rate during activation compared with control. The cells that enhanced their firing rate (n = 8) had a spontaneous firing rate
of 5.6 ± 2 Hz during control conditions and 16.2 ± 3 Hz
during activation (t test; p < 0.001),
whereas those remaining (n = 15) had a firing rate of
2.1 ± 1 Hz during control and 0.6 ± 0.2 Hz during
activation (t test; p < 0.01).
After determining the principal whisker corresponding to the recorded
neuron and an adjacent whisker that also discharged the neuron, a
baseline was obtained under control conditions (n = 60-100 trials per whisker). This yielded a large short-latency response to the principal whisker and a smaller and longer-latency response to the adjacent whisker. Figure
2 presents an example of a cell recorded
at 720 µm in depth in the barrel cortex. The cell responded robustly
to the principal whisker and also to an adjacent whisker (Fig.
2A). Stimulation of the brainstem reticular formation
reduced the spontaneous firing rate of this neuron and also reduced the
sensory responses to the principal and the adjacent whiskers. However,
whereas the response to the adjacent whisker was virtually eliminated,
the response to the principal whisker was still salient. Consequently,
a strong selectivity of the response for the principal whisker
resulted, i.e., during aroused states of the brain, cortical neurons
become more selective for their principal inputs. Among the recorded
neurons, several (n = 5) displayed features that are
consistent with inhibitory interneurons (Swadlow, 1995). These
suspected interneurons responded with a high-frequency burst to whisker
stimulation and displayed short spike durations. Interestingly, the
sensory response of these neurons was also focused by activation.
Figure 3 presents an example of a
response from a presumed interneuron located at 690 µm in depth. The
cell responded robustly to the principal whisker and also to the
adjacent whisker during quiescent states. After activation induced by
stimulating the brainstem reticular formation, this neuron enhanced its
spontaneous firing rate, whereas the response to both the principal and
adjacent whiskers were suppressed. However, the response
suppression resulted in the complete elimination of the response to
the adjacent whisker, whereas the response to the principal whisker was
still present. Thus, presumed interneurons also enhance their
selectivity during arousal as a consequence of sensory suppression.
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Figure 2.
Enhanced selectivity of a neuron in layers IV-III
of barrel cortex during activation. Effect of activation induced by
stimulating the brainstem reticular formation on single-unit response
to stimulation of the principal whisker and of an adjacent whisker.
Single-unit responses are displayed as the probability of firing per 2 msec bins before (top) and during
(bottom) activation (RF Stim.). The
whisker stimulus is delivered at time 0.
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Figure 3.
Enhanced selectivity of a presumed inhibitory
interneuron in layers IV-III of barrel cortex during activation.
Effect of activation induced by stimulating the brainstem reticular
formation on single-unit response to stimulation of the principal
whisker (left) and of an adjacent whisker
(right). Single-unit responses are displayed as the
probability of firing per 2 msec bins before (top) and
during (bottom) activation (RF Stim.).
The whisker stimulus is delivered at time 0.
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Figure 4 presents population data for the
cells in the study (n = 23). For the cells tested in
layers IV-III, the response to the principal whisker was reduced by
26.6 ± 3% (t test; p < 0.001),
whereas the response to the adjacent whisker was reduced by 87.5 ± 2% (t test; p < 0.0001) (Fig.
4A). As a consequence of the much stronger reduction
in the response to the adjacent whisker, the response of the neurons
became selective for the principal whisker. This selectivity was
further assessed by calculating a ratio (AD/PW)
between the response to the adjacent whisker and the principal whisker
(Fig. 4B). Under control conditions, the mean ratio
was 0.47 ± 0.08. However, during activation caused by stimulating
the brainstem reticular formation, the ratio was reduced to 0.08 ± 0.02, indicating that the preference for the principal whisker
increased significantly (t test; p < 0.0001). Figure 4C displays a scatterplot for the principal
whisker response for each neuron plotted versus its adjacent
whisker response under control conditions (open squares) and
during activation caused by stimulating the brainstem reticular
formation (filled circles). A regression line is used
to fit each group of data. The responses to both adjacent and principal
whiskers were reduced during activation. However, the response to the
adjacent whisker was almost eliminated for most of the cells recorded.
Thus, the cells became selective for the principal whisker.
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Figure 4.
Population data showing the enhanced selectivity
of neurons in layers IV-III of barrel cortex during activation.
A, Mean effect of activation induced by stimulating the
brainstem reticular formation on the response of single units
(n = 23) to stimulation of the principal whisker
(PW) and of an adjacent whisker
(AW). B, Ratio of the adjacent
whisker and principal whisker responses during control conditions and
during activation caused by stimulating the brainstem reticular
formation (RF Stim.). C, Scatterplot for
each single unit displaying the principal whisker response plotted
versus the adjacent whisker response under control conditions
(open squares) and during activation caused by
stimulating the brainstem reticular formation (filled
circles). A regression line is used to fit each group of
data.
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DISCUSSION |
The present study found that, because of sensory suppression, the
horizontal spread of activity in the neocortex from the thalamocortical
recipient area is strongly suppressed during activated states,
resulting in the focusing of cortical sensory representations and
receptive fields. Thus, during aroused states, thalamocortical suppression serves as a mechanism to focus sensory inputs to their appropriate representations (barrels) in neocortex, which may be
helpful for the spatial processing of sensory information.
This focusing may be helpful for sensory processing because the lack of
selectivity observed during quiescent states seems to hinder
information processing. For example, simple tasks performed by the
somatosensory system (e.g., two-point discrimination) are more
difficult to conceive with such overlapping and large cortical representations and receptive fields. Obviously, these behavioral capacities are possible only during brain-activated states typical of
alertness, attention, and arousal and not during quiescent states
typical of drowsiness, inattentiveness, and sleep. Thus, to understand
how these behavioral capacities are executed, it is important to study
the properties of neural circuits during brain-activated states typical
of arousal and information processing. Cortical sensory suppression
during arousal may serve to focus sensory inputs to allow a more
discreet and segregate representation of sensory information in the neocortex.
The activity-dependent suppression of the thalamocortical connection
during arousal may work together with recurrent cortical inhibition to
produce the effects described in the present study. Locally recurrent
inhibition has been proposed as the means to achieve selectivity in the
neocortex (Simons, 1985; Miller et al., 2001). In fact, thalamocortical
neurons produce a very powerful connection with cortical inhibitory
interneurons (Swadlow, 1995), much more so than with excitatory neurons
of layer IV (Gibson et al., 1999). Although the efficacy of the
thalamocortical connection with interneurons is reduced during aroused
states (Swadlow and Gusev, 2001; Castro-Alamancos and Oldford, 2002),
it should still be effective in producing inhibitory potentials and
reducing the spread of activity. In fact, one of the main consequences
of stimulating the brainstem reticular formation is a reduction of the
spontaneous firing rate of a large percentage of cortical neurons
(Castro-Alamancos and Oldford, 2002). This is consistent with the
hyperpolarization of cortical neurons via the activation of
GABAA receptors. One possibility is that the
enhanced firing rates of thalamocortical neurons during arousal
increase the firing of cortical inhibitory interneurons that are
strongly innervated by thalamocortical inputs (White and Rock, 1981).
This would result in an enhanced tonic level of recurrent inhibition in
the neocortex during activated states. Therefore, thalamocortical
suppression and enhanced cortical inhibition during arousal, which are
both a direct consequence of enhanced thalamocortical firing, result in
the increased selectivity (focusing) of cortical receptive fields and
sensory representations.
Previous work has shown that, when receptive fields obtained during
anesthesia are compared with those of waking animals, important
transformations are observed. Some studies have shown that the size of
cortical receptive fields increase as the depth of anesthesia is
lessened from very deep levels (Armstrong-James and George, 1988).
Furthermore, when urethane anesthesia was compared with waking, neurons
in the thalamocortical recipient layer (i.e., layer IV) had smaller
receptive fields during waking compared with anesthesia, as indicated
by multiunit recordings and comparing different cells in both states
(Simons et al., 1992). In the visual system, cortical neurons also seem
to reduce the size of their receptive fields during arousal (Worgotter
et al., 1998). In the auditory system, different neurons undergo a
variety of changes in receptive field size (Edeline et al., 2001).
Also, in the auditory cortex, neurons undergo dramatic changes in
receptive fields, so that after behavioral conditioning receptive
fields enhance their response to the behaviorally relevant stimulus and
reduce their response to other irrelevant stimuli (Weinberger, 1995). Although the present study was performed in urethane-anesthetized animals, it is important to point out that the thalamocortical responsiveness observed here during control versus activation states
highly resembles the sleep-quiescent versus active exploration states
in freely behaving animals (Castro-Alamancos and Oldford, 2002). Thus,
thalamocortical suppression is present in freely behaving animals
during activated states, an effect that is mimicked in anesthetized
animals by stimulating the brainstem reticular formation.
In conclusion, increased thalamocortical tonic firing during activation
reduces the strength of the thalamocortical connection and may increase
tonic cortical inhibition. Under these conditions, the response of
cortical neurons to sensory inputs becomes more selective for their
principal input. Thus, cortical representations and receptive fields
become focused during arousal.
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FOOTNOTES |
Received July 29, 2002; revised Aug. 23, 2002; accepted Sept. 3, 2002.
This work was supported by the Medical Research Council of Canada,
Natural Sciences and Engineering Council of Canada, Fonds de la
Recherche en Santé du Quebec, Canadian Foundation for Innovation, and Savoy Foundation. Multichannel silicon probes were provided by the
University of Michigan Center for Neural Communication Technology
sponsored by National Institutes of Health National Center for Research
Resources. Thanks to Dan Simons and Harvey Swadlow for helpful comments.
Correspondence should be addressed to Dr. Manuel Castro-Alamancos,
Montreal Neurological Institute, 3801 University Street, Room WB210,
Montreal, Quebec H3A 2B4 Canada. E-mail: manuel.castro{at}mcgill.ca.
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ABSTRACT
INTRODUCTION
