Theme : Dreams
Coalescence of Sleep Rhythms and Their Chronology in Corticothalamic
Networks
Mircea Steriade and Florin Amzica
Laboratoire de Neurophysiologie, Faculté de Médicine,
Université Laval, Quebec G1K 7P4, Canada
Abstract
The cellular substrates of sleep oscillations have recently been investigated
by means of multi-site, intracellular and extracellular recordings under
anesthesia, and these data have been validated during natural sleep in
cats and humans. Although various rhythms occurring during the state of
resting sleep (spindle, 7-14 Hz; delta, 1-4 Hz; and slow oscillation,
<1 Hz) are conventionally described by using their different frequencies,
they are coalesced within complex wave-sequences due to the synchronizing
power of the cortically generated slow oscillation (main peak around 0.7
Hz). In intracellular recordings from anesthetized animals, the slow oscillation
is characterized by a biphasic sequence consisting of a prolonged hyperpolarization
and depolarization. Basically similar patterns are observed by means of
extracellular discharges and/or field potentials in naturally sleeping
animals and humans. The depolarizing component of the slow oscillation
is transferred to the thalamus where it contributes to the synchronization
of spindles over widespread territories. The association between the depolarizing
component of the slow oscillation and the subsequent sequence of spindle
waves forms what is termed the K-complex. The slow oscillation also groups
cortically generated delta waves. At variance with previous assumptions
that the brain lies for the most part in the dark and a global inhibition
occurs in resting sleep, cortical cells are quite active in this behavioral
state. This unexpectedly rich activity raises the possibility that, during
sleep, the brain is occupied to specify/reorganize circuits and to consolidate
memory traces acquired during wakefulness.
Current Claim: During quiescent sleep, low- and high-frequency thalamic
and cortical rhythms are grouped into complex wave-sequences due to the
depolarizing component of a cortically generated slow oscillation.
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This paper is an attempt at revising the current thinking on the generation
and synchronization of various oscillations that define the state of resting
(non-REM) sleep at the EEG level. We present three main points. (A) A
novel slow oscillation, described in intracellular recordings from cortical
and thalamic neurons (Steriade et al., 1993a, 1993c, 1993d), has the virtue
of grouping other sleep rhythms, spindles and delta, into complex wave-sequences.
The slow oscillation has a frequency of about 0.6 to 1 Hz in ketamine-anesthetized
as well as naturally sleeping animals (Steriade et al., 1996a, 1996b)
and humans (Steriade et al., 1993c; Achermann and Borbély, 1997;
Amzica and Steriade, 1997a). Instead of considering different sleep oscillatory
types as generated within isolated networks, we envision the cerebral
cortex and thalamus as a unified oscillatory machine in which the depolarizing
component of the cortically generated slow oscillation drives thalamic
reticular (RE) and thalamocortical (TC) cells to produce spindles (7-14
Hz) and a clock-like component of delta waves (1-4 Hz). The generation
of slow oscillation within the neocortex has been demonstrated by its
survival in cortex after thalamectomy (Steriade et al., 1993d), its disruption
by disconnection of intracortical synaptic linkages (Amzica and Steriade,
1995b), and its absence in the thalamus of decorticated animals (Timofeev
and Steriade, 1996). However, in intact animals the slow oscillation is
reflected in the thalamus by both RE and TC cells. This contributes to
the grouping of thalamically generated oscillations (spindles and clock-like
delta). (B) The combination of the excitatory component of the slow oscillation
with spindles leads to the appearance of sleep K-complexes in both cats
and humans (Amzica and Steriade, 1997a, 1997b). (C) The orderly appearance
of various rhythms throughout the state of resting sleep, under the umbrella
of the slow oscillation, is associated with a progressive increase in
the corticothalamic coherence of sleep rhythms.
Why is it important to study the neuronal substrates underlying spontaneous
brain rhythms even if their functional significance is far from being
elucidated? Although different EEG oscillatory types were described by
British and Eastern European investigators more than a century ago, their
cellular bases have only been revealed during the past 10 to 15 years.
Since the mid-1980s, the apparent chaos of EEG waves has been reduced
to a few basic cellular operations that shed light on the origin and mechanisms
generating various EEG grapho-elements. Our reductionistic attempt provides
explanations of the mechanisms underlying brain rhythms and may ultimately
shed light on the functional role played by these oscillations. To give
just one example: some still describe different types of EEG sleep spindles,
with lower or higher frequencies, while intracellular data allow us to
understand that these supposedly different types are attributable to a
single event, namely, the duration of hyperpolarization-rebound sequence
in TC neurons. The hyperpolarization de-inactivates a low-threshold Ca2+-mediated
current, underlying postinihibitory rebound spike-bursts that are transferred
to cortical areas (Steriade and Llinás, 1988). If the hyperpolarization
is of about 70 msec, the spindle frequency is about 14-15 Hz; if the hyperpolarization
is longer because its progenitors, GABAergic RE neurons, fire longer spike-bursts,
the frequency is lower. Understanding that the spindle oscillation is
due to rhythmic inhibitory postsynaptic potentials (IPSPs) generated by
RE neurons (Steriade et al., 1985; Bal et al., 1995) may explain one of
their functional roles, which is the blockade of synaptic transmission
through the thalamus (Steriade et al., 1969; Timofeev et al., 1996), thus
deafferenting the cortex from the outside world and allowing a peaceful
sleep. Similar examples may be taken from the study of other brain oscillations
defining resting sleep.
The aim of the present paper is to reveal the cellular substrates of
sleep oscillations and to propose some avenues to understand their functions.
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Data reported in this paper result from intracellular recordings (in some
cases dual simultaneous impalements of cortical neurons or cortical and
thalamic neurons) in conjunction with multi-site extracellular recordings
in acutely prepared cats under different types of anesthesia (mainly ketamine-xylazine)
or from multi-site extracellular recordings during natural wake and sleep
states in chronically implanted cats (see technical details in Steriade
et al., 1996a, 1996b). The intrinsic properties and input-output organization
of different cortical and thalamic neuronal types were defined by standard
electrophysiological procedures (depolarizing and hyperpolarizing current
pulses at different levels of membrane potential - Vm, antidromic and
orthodromic responses) and the morphological features of recorded neurons
were known by intracellular staining with Lucifer yellow or Neurobiotin
(see Steriade et al., 1993c; Contreras and Steriade, 1995). The results
from intracellular recordings are based on neurons with resting Vm more
negative than -55 mV and overshooting action potentials. Different analyses
used to assess the synchronization processes were cross-correlograms,
measures of synchrony coefficient, wave-triggered excitatory postsynaptic
potentials (EPSPs), spike-triggered-averages, first-spike-analysis, and
sequential field correlations as visualized by three-dimensional surfaces
and contour maps (see Steriade and Amzica, 1994; Amzica and Steriade,
1995a, 1995b).
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Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Coalescence of three types of sleep rhythms grouped by the cortical slow
oscillation
For didactic purposes, three types of oscillations are usually described
as characterizing the state of resting sleep: spindles (7-14 Hz), delta
(1-4 Hz) and slow oscillation (below 1 Hz, usually 0.6 to 1 Hz). However,
in brain-intact animals and humans, the sleep oscillations are not seen
in isolation but they are grouped by the recently discovered slow oscillation.
Figure 1 shows that the intracellularly recorded slow oscillation (0.8-0.9
Hz) progressively develops in conjunction with the increased synchronization
of EEG field potentials. This development is associated with steeper slopes
of both depolarizing and hyperpolarizing components of the slow oscillation
(compare 1 to 2 in bottom panels). The depolarizing components of the
slow oscillation, reflected as a sharp depth-negative field potential
(Figs. 1 and 2A), give rise to corticothalamic volleys that, by driving
thalamic neurons, induce brief sequences of spindle waves consisting of
rhythmic IPSPs in TC cells. The amplitudes of spindle-related IPSPs in
TC cells, which increase under steady depolarization (Fig. 2B), are induced
by spike-bursts in GABAergic RE cells that, in turn, are driven by the
depolarizing component of the cortical slow oscillation (Steriade et al.,
1993a; Contreras and Steriade, 1995). Distinctly from the waxing-and-waning
pattern of spindle oscillations in the decorticated animals or under barbiturate
anesthesia when cortical neurons display reduced spontaneous activities,
the spindles triggered by the corticothalamic volley of the slow oscillation
under ketamine-xylazine anesthesia are shorter and display an exclusively
waning pattern (Fig. 2A-B). This is due to the fact that the synchronous
excitation of corticothalamic neurons during the slow oscillation entrain,
right from the start, a great population of neurons implicated in the
genesis of spindles within a thalamic territory, thus explaining the absence
of an initial waxing process (Contreras and Steriade, 1996).
The coalescence of the slow and spindle oscillations is especially visible
during light sleep. The evolution of sleep rhythms, with their progressively
increased amplitudes from the end of waking state toward the end of deep
resting sleep, is illustrated by means of multi-site recordings in Fig.
3 which shows that, in naturally sleeping animals, the slow oscillation
dominates brain electrical activity throughout the state of resting sleep.
During light sleep, every cycle of the slow oscillation generally leads
to a sequence of spindle waves, on one, another, or all cortical leads.
As shown above (Fig. 2), this is due to the synaptic engagement of thalamic
neurons implicated in spindle genesis. Notably, though deep sleep displays
less spindles, toward the end of deep sleep, just before EEG activation
occurs in REM sleep, spindles recover their power, as during the initial
stages of resting sleep (Fig. 3). This can be explained by the voltage-dependency
of sleep rhythms in TC cells. Indeed, at the single-cell level, spindles
occur at the resting Vm of TC neurons, whereas, at more hyperpolarized
levels, spindles are progressively replaced by intrinsically generated,
clock-like delta potentials (Steriade et al., 1991; Nuñez et al.,
1992). These intracellular data from anesthetized preparations found support
in results obtained in naturally sleeping animals, showing that thalamic
spindles are maximal at sleep onset and decrease thereafter, whereas thalamic
delta waves increase gradually during resting sleep (Lancel et al., 1992).
Thus, with increasing hyperpolarization of TC cells during resting sleep,
due to the progressive diminished firing rates of cholinergic and other
types of brainstem-thalamic activating neurons (reviewed in Steriade and
McCarley, 1990), the incidence and amplitude of spindles are largely diminished
during deep sleep stages. On the other hand, the reappearance of spindles
toward the end of resting sleep (see Fig. 3) is attributable to a relative
depolarization of TC cells, due to the increased firing rates of brainstem-thalamic
reticular neurons that display precursor-increased rates of spontaneous
firing, 30 to 60 s before the onset of REM sleep (Steriade et al., 1990).
Spindling is not the only sleep rhythm that is modulated and grouped
by the cortical slow oscillation. (A) The intrinsically generated delta
rhythm of TC cells is influenced by the slow oscillation because the rhythmic
depolarizing corticothalamic drives increase the membrane conductance
of TC cells and prevent the interplay between a hyperpolarization-activated
cation current (Ih) and a calcium current de-inactivated by membrane hyperpolarization
(It), thus periodically dampening the slow oscillation (see Fig. 10A in
Steriade et al., 1993a; and Box 1 in Steriade et al., 1994). However,
as corticothalamic volleys also drive GABAergic RE neurons, singly delta-oscillating
TC cells may be synchronized because RE cells set their Vm at the adequate
level where delta rhythm is generated (Steriade et al., 1991). (B) The
other component of delta waves, that is generated intracortically after
thalamectomy (see above), has not yet been systematically studied at the
intracellular level to shed light on its neuronal substrate(s). One possibility
is that the frequency band of 1-4 Hz in the power spectrum during late
stages of resting sleep results, at least partially, from the shape of
the depth-negative (depolarizing) component of the slow oscillation (0.3-0.4
s), which represents the K-complex (Amzica and Steriade, 1997a, 1997b).
Anyway, typical delta waves, at a frequency of 2-4 Hz, generated by both
regular-spiking and intrinsically bursting cortical neurons, are grouped
within sequences recurring with the slow rhythm (see Fig. 3 in Steriade
et al., 1993d). And, in human sleep EEG, sequential mean amplitudes of
delta waves show their periodic recurrence with the rhythm of slow oscillation
(Steriade et al., 1993c). That delta and slow oscillation represent two
distinct phenomena was recently demonstrated by Achermann and Borbély
(1997) who showed differences in the dynamics between the slow and the
delta oscillations, as the latter declines in activity from the first
to the second non-REM sleep episode, whereas the former does not. The
current confusion in the literature between delta oscillation and delta
waves is probably due to the fact that the presence of a peak in power
spectrum may result from an oscillation with the frequency of the peak
and/or a frequent occurrence of waves with a duration and shape that would
contribute to that particular peak.
We investigated the synchronization of slow oscillation in naturally
sleeping animals by using the wavelet procedure that detects waveforms
similar in shape with a preset pattern. Thus, the original EEG trace is
digitally filtered and tranformed into a new time series (signal) that
conserves from the original only the relevant wavelets (Amzica and Steriade,
1997a). In order to match K-complexes (see below), we used Daubechies'
wavelets (Daubechies, 1988). Figure 4 shows that the intracortical as
well as corticothalamic synchronization of the slow oscillation is most
obvious during deep sleep and is best expressed among areas across the
same gyrus (areas 5 and 7) or among cortical areas and related thalamic
nuclei (area 7 and rostral intralaminar nuclei). However, synchronization
is also seen between morphologically distant and functionally different
cortical fields (motor area 4 and visual area 18).
Finally, because the slow oscillation was first described intracellularly
under different anesthetics, we had to validate the similarity of these
cellular patterns to those observed extracellularly in chronically implanted,
unanesthetized animals. Under both ketamine-xylazine anesthesia and natural
sleep, the slow oscillation has a frequency of 0.6 to 1 Hz (Fig. 5A-B).
Under anesthesia, the field potentials associated with this oscillation
are prolonged depth-positive (hyperpolarizing) and depth-negative (depolarizing)
components (Fig. 5A). Similar aspects are observed in natural resting
sleep, when the depth-positive waves are accompanied by silenced firing,
while depth-negative sharp deflections are associated with brisk firing
(Fig. 5B). Surprisingly, because fast oscillations (generally 20-50 Hz)
are conventionally associated with brain-activated states, similar fast
oscillations also appear during resting sleep but are selectively obliterated
during the depth-positive component of the slow oscillation (see inset
in Fig. 5B). This demonstrates the voltage(depolarization)-dependency
of fast oscillations.
The slow oscillation and K-complexes in human sleep
After preliminary data showing the presence of slow oscillation during
natural sleep in humans (Steriade et al., 1993c), the human slow oscillation
(<1 Hz) was recently reported in parallel studies from two laboratories
(Achermann and Borbély, 1997; Amzica and Steriade, 1997a). Here,
we document different aspects of the human slow sleep oscillation. (A)
During stage 2, scalp recordings show a prevalent peak (0.8 Hz) within
the frequency range of the slow oscillation as well as a minor mode around
15 Hz reflecting spindle waves (Fig. 6). The depth-negative components
of the slow oscillation, followed or not by spindles, represent the K-complexes
(bottom panels in Fig. 6). The frequency of K-complexes (peaks at 0.5
Hz in stage 2, 0.7 Hz in stages 3-4 of human sleep) is very similar, up
to identity, to the frequency of the slow oscillation during natural sleep
(see Fig. 2C in Amzica and Steriade, 1997a). (B) The power spectrum reveals
a major peak around 1 Hz, that becomes evident from stage 2 and continues
throughout resting sleep (top panel in Fig. 7). The slow oscillation is
particularly abundant in fronto-parietal leads (bottom panel in Fig. 7).
These data invite human sleep researchers to consider the two types of
oscillatory activities below 4 Hz (delta, 1-4 Hz; slow, <1 Hz) and,
accordingly, to analyze their results by taking into account the distinctness
of these two oscillations, as demonstrated by Achermann and Borbély
(1997; see above).
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Figure 1
Figure 5
Figure 7
Cellular mechanisms of sleep oscillations
Sequences of spindle waves, recurring with a slow rhythm at about 0.3-0.5
Hz, occur during early sleep stages and are generated by interactions
between RE and TC neurons (Steriade et al., 1993b; Bal et al., 1995).
The pacemaking role of RE neurons was shown by abolition of spindles in
TC systems after disconnection from RE nucleus (Steriade et al., 1985)
and by preservation of spindles in the deafferented rostral pole of the
RE nucleus (Steriade et al., 1987). Although spindles are generated in
the thalamus after decortication (Morison and Bassett, 1945), corticothalamic
volleys are important in triggering and synchronizing spindles throughout
TC systems (Steriade et al., 1972; Contreras et al., 1996a, 1997).
Delta waves, usually regarded as a single type of EEG waves, consist of
two components. The cortical one survives thalamectomy (Villablanca, 1974;
Steriade et al., 1993d). The thalamic-generated delta oscillation is present
after decortication (Curró Dossi et al., 1992), is stereotyped
and clock-like, and its intrinsic-cell nature is due to the interplay
of two hyperpolarization-activated currents of TC neurons, Ih and It (McCormick
and Pape, 1990; Soltesz et al., 1991).
The basic features of the recently described slow oscillation (see Introduction)
consist of a prolonged hyperpolarization (up to 1 s), associated with
a depth-positive (surface-negative) EEG wave, followed by a long-lasting
depolarization (up to 0.8 s), associated with a depth-negative (surface-positive)
field potential. These sequences recur periodically, with a rhythm of
0.6 to 1 Hz. The long-lasting depolarization consists of EPSPs, fast prepotentials
(FPPs) and fast IPSPs reflecting the action of synaptically coupled GABAergic
local-circuit cells; in addition, the depolarizing component is made up
of both NMDA-mediated synaptic excitatory events and a voltage-dependent
persistent Na+ current, as the depolarizing envelope is shortened by adminstration
of ketamine, an NMDA blocker, or intracellular injection of QX-314, a
blocker of Na+ currents (Steriade et al., 1993c). The prolonged hyperpolarization
results from a series of factors; among them, disfacilitation in cortical
networks is probably the most important (Contreras et al., 1996b).
Possible significance of sleep rhythms
The frenzied activity of cortical neurons during the slow oscillation,
occurring in natural sleep or deep anesthesia (see Figs. 1 and 5) during
which consciousness is conventionally thought to be annihilated, prompts
us to consider different roles played by the rhythmic bombardment of thalamic
and cortical neurons upon their targets. Indeed, the deafferentation of
thalamocortical networks produced by the spindle-related IPSPs in TC cells,
with the consequence of obliterating incoming messages and thus disconnecting
the brain from the outside world, is probably not the only effect of sleep
oscillations. To begin with, whereas TC cells do not transmit ascending
afferent signals to cortex during the hyperpolarizing phase of the slow
oscillation because the EPSPs do not reach firing threshold, the internal
dialogue of the brain (as tested by corticocortical and corticothalamic
volleys) is not disrupted during this hyperpolarizing phase (Timofeev
et al., 1996). The preservation, during resting sleep, of this form of
internal communication is reminiscent of earlier data showing that callosally
evoked discharges in precentral neurons of behaving monkeys are not diminished
from waking to resting sleep and may even be enhanced (Steriade et al.,
1974).
The state of resting sleep may subserve even more noble functions during
different oscillatory activities of thalamic and cortical neurons. Rhythmic
activation of cortical neurons, produced by repetitive spike-bursts of
TC cells during sleep spindles, are hypothesized to reinforce and/or specify
the circuitry, to stimulate dendrites to grow more spines, and to contribute
to the consolidation of memory traces acquired during wakefulness (Steriade
et al., 1993a). The idea of such plastic changes may be tested by using
procedures of cellular conditioning and by lesioning different structures
implicated in the production of sleep oscillations. For example, the effects
of abolishing spindles in a hemisphere, after chemical lesioning of the
RE nucleus (Steriade et al., 1985), may be investigated upon the time
required for establishing conditioned responses in the ipsilateral cortex
devoid of spindles. That spindles and their artificial model, augmenting
responses evoked by low-frequency (10 Hz) repetitive volleys, are able
to produce short-term plasticity was demonstrated even in the thalamus
of decorticated animals (Steriade and Timofeev, 1997). In these experiments,
intrathalamic stimulation at 10 Hz produced a progressive and persistent
increase in slow depolarizing responses of TC cells, as well as to a persistent
and prolonged decrease in the amplitudes of the IPSPs. Even more pronounced
plastic changes are expected to occur with augmenting responses in an
animal with intact cortex (Morison and Dempsey, 1943; Morin and Steriade,
1981; Castro-Alamancos and Connors, 1996) since augmenting does not lead
to prolonged paroxysmal developments in decorticated animals but such
transformations can occur in the presence of intact thalamocorticothalamic
loops (unpublished data). After a series of repetitive responses in bursting
thalamic neurons, evoked by cortical volleys at 10 Hz, the neurons spontaneously
produced spike-bursts very similar to the shape and frequencies of those
evoked stimuli (see Fig. 7 in Steriade, 1991). The "memory"
of the circuit, presumably due to resonant frequencies in the thalamus
and neocortex, may eventually lead to paroxysmal events, consisting of
spike-wave seizures at 2-4 Hz (Steriade et al., 1976).
Thus, synapses within intracortical and thalamocortical circuits may
be thought of as dynamically stabilized by internally generated, apparently
"non-utilitarian" excitations during sleep oscillations (see
Kavanau, 1994). The "rehearsal", in resting sleep, of information
acquired during active behavior (Buzsáki, 1989; Wilson and McNaughton,
1994) is also revealed by the persistence, during periods of subsequent
sleep, of intracortical and corticothalamic synchrony of fast (gamma)
oscillations acquired during conditioning sessions (Amzica et al., 1997).
All these data suggest that the re-expression of information during sleep
may be related to memory consolidation.
1. Achermann P, Borbély AA. Low-frequency (<1 Hz) oscillations
in the human sleep EEG. Neuroscience 1997; 81: 213-22.
2. Amzica F, Steriade M. Short- and long-range synchronization of the
slow (<1 Hz) cortical oscillation. J Neurophysiol 1995a; 73: 20-38.
3. Amzica F, Steriade M. Disconnection of intracortical synaptic linkages
disrupts synchronization of a slow oscillation. J Neurosci 1995b; 15:
4658-77.
4. Amzica F, Steriade M. The K-complex: its slow (<1 Hz) rhythmicity
and relation with delta waves. Neurology 1997a; 49: 952-9.
5. Amzica F, Steriade M. Cellular substrates and laminar profile of sleep
K-complex. Neuroscience 1997b; 82: 671-86.
6. Amzica F, Neckelmann D, Steriade M. Instrumental conditioning of fast
(20- to 50-Hz) oscillations in corticothalamic networks. Proc Natl Acad
Sci USA 1997; 94: 1985-9.
7. Bal T, von Krosigk M, McCormick DA. Role of the ferret perigeniculate
nucleus in the generation of synchronized oscillations in vitro. J Physiol
Lond 1995; 483: 665-85.
8. Buzsáki G. Two-stage model of memory trace formation: a role
for "noisy" brain states. Neuroscience 1989; 31: 551-70.
9. Castro-Alamancos MA, Connors BW. Cellular mechanisms of the augmenting
response: short-term plasticity in a thalamocortical pathway. J Neurosci
1996; 16: 7742-56.
10. Contreras D, Steriade M. Cellular basis of EEG slow rhythms: a study
of dynamic corticothalamic relationships. J Neurosci 1995; 15: 604-22.
11. Contreras D, Steriade M. Spindle oscillations in cats: the role of
corticothalamic feedback in a thalamically generated rhythm. J Physiol
Lond 1996; 490: 159-80.
12. Contreras D, Destexhe A, Sejnowski TJ, Steriade M. Control of spatiotemporal
coherence of a thalamic oscillation by corticothalamic feedback. Science
1996a; 274: 771-4.
13. Contreras D, Timofeev I, Steriade M. Mechanisms of long-lasting hyperpolarizations
underlying slow sleep oscillations in cat corticothalamic networks. J
Physiol Lond 1996b; 494: 251-64.
14. Contreras D, Destexhe A, Sejnowski TJ, Steriade M. Spatiotemporal
patterns of spindle oscillations in cortex and thalamus. J Neurosci 1997;
17: 1179-96.
15. Curró Dossi R, Nuñez A, Steriade M. Electrophysiology
of a slow (0.5-4 Hz) intrinsic oscillation of cat thalamocortical neurones
in vivo. J Physiol Lond 1992; 447: 215-34.
16. Daubechies I. Orthonormal bases of compactly supported wavelets.
Commun Pure Appl Math 1988; 41: 909-96.
17. Kavanau JL. Sleep and dynamic stabilization of neural circuitry:
a review and synthesis. Behav Brain Res 1994; 63: 111-26.
18. Lancel M, van Riezen H, Glatt A. The time course of sigma activity
and slow wave activity during NREMs in cortical and thalamic EEG of the
cat during baseline and after 12 hours of wakefulness. Brain Res 1992;
596: 286-95.
19. McCormick DA, Pape HC. Properties of a hyperpolarization-activated
cation current and its role in rhythmic oscillation in thalamic relay
neurones. J Physiol Lond 1990; 431: 291-318.
20. Morin D, Steriade M. Development from primary to augmenting responses
in primary somatosensory cortex. Brain Res 1981; 205: 49-66.
21. Morison RS, Bassett DL. Electrical activity of the thalamus and basal
ganglia in decorticate cats. J Neurophysiol 1945; 8: 309-14.
22. Morison RS, Dempsey EW. Mechanism of thalamocortical augmentation
and repetition. Am J Physiol 1943; 138: 297-308.
23. Nuñez A, Curró Dossi R, Contreras D, Steriade M. Intracellular
evidence for incompatibility between spindle and delta oscillations in
thalamocortical neurons of cat. Neuroscience 1992; 48: 75-85.
24. Soltesz I, Lightowler S, Leresche N, Jassik-Gerschenfeld D, Pollard
CE, Crunelli V. Two inward currents and the transformation of low-frequency
oscillations of rat and cat thalamocortical cells. J Physiol Lond 1991;
441: 175-97.
25. Steriade M. Alertness, quiet sleep, dreaming. In: A Peters, EG Jones,
eds. Cerebral Cortex, vol. 9, Normal and Altered States of Function. New
York: Plenum Press, 1991, pp. 279-357.
26. Steriade M, Amzica F. Dynamic coupling among neocortical neurons
during evoked and spontaneous spike-wave seizure activity. J Neurophysiol
1994; 72: 2051-69.
27. Steriade M, Llinás RR. The functional states of the thalamus
and the associated neuronal interplay. Physiol Rev 1988; 68: 649-742.
28. Steriade M, McCarley RW. Brainstem Control of Wakefulness and Sleep.
New York: Plenum Press, 1990.
29. Steriade M, Timofeev I. Short-term plasticity during intrathalamic
augmenting responses in decorticated cats. J Neurosci 1997; 17: 3778-95.
30. Steriade M, Iosif G, Apostol V. Responsiveness of thalamic and cortical
motor relays during arousal and various stages of sleep. J Neurophysiol
1969; 32: 251-65.
31. Steriade M, Wyzinski P, Apostol V. Corticofugal projections governing
rhythmic thalamic activity. In: TL Frigyesi, E Rinvik, MD Yahr, eds. Corticothalamic
Projections and Sensorimotor Activities. New York: Raven Press, 1972,
pp. 221-72.
32. Steriade M, Deschênes M, Wyzinski P, Hallé JY. Input-output
organization of the motor cortex and its alterations during sleep and
waking. In: O Petre-Quadens, JD Schlag, eds. Basic Sleep Mechanisms. New
York: Academic Press, 1974, pp. 143-203.
33. Steriade M, Oakson G, Diallo A. Cortically elicited spike-wave afterdischarges
in thalamic neurons. Electroencephalogr Clin Neurophysiol 1976; 41: 641-4.
34. Steriade M, Deschênes M, Domich L, Mulle C. Abolition of spindle
oscillations in thalamic neurons disconnected from nucleus reticularis
thalami. J Neurophysiol 1985; 54: 1473-97.
35. Steriade M, Domich L, Oakson G, Deschênes M. The deafferented
reticularis thalamic nucleus generates spindle rhythmicity. J Neurophysiol
1987; 57: 260-73.
36. Steriade M, Datta S, Paré D, Oakson G, Curró Dossi
R. Neuronal activities in brain-stem cholinergic nuclei related to tonic
activation processes in thalamocortical systems. J Neurosci 1990; 10:
2541-59.
37. Steriade M, Curró Dossi R, Nuñez A. Network modulation
of a slow intrinsic oscillation of cat thalamocortical neurons implicated
in sleep delta waves: cortically induced synchronization and brainstem
cholinergic suppression. J Neurosci 1991; 11: 3200-17.
38. Steriade M, Contreras D, Curró Dossi R, Nuñez A. The
slow (<1 Hz) oscillation in reticular thalamic and thalamocortical
neurons: scenario of sleep rhythm generation in interacting thalamic and
neocortical networks. J Neurosci 1993a; 13: 3284-99.
39. Steriade M, McCormick DA, Sejnowski TJ. Thalamocortical oscillations
in the sleeping and aroused brain. Science 1993b; 262: 679-85.
40. Steriade M, Nuñez A, Amzica F. A novel slow (<1 Hz) oscillation
of neocortical neurons in vivo: depolarizing and hyperpolarizing components.
J Neurosci 1993c; 13: 3252-65.
41. Steriade M, Nuñez A, Amzica F. Intracellular analysis of relations
between the slow (<1 Hz) neocortical oscillation and other sleep rhythms
of the electroencephalogram. J Neurosci 1993d; 13: 3266-83.
42. Steriade M, Contreras D, Amzica F. Synchronized sleep oscillations
and their paroxysmal developments. Trends Neurosci 1994; 17: 199-208.
43. Steriade M, Amzica F, Contreras D. Synchronization of fast (30-40
Hz) spontaneous cortical rhythms during brain activation. J Neurosci 1996a;
16: 392-417.
44. Steriade M, Contreras D, Amzica F, Timofeev I. Synchronization of
fast (30-40 Hz) spontaneous oscillations in intrathalamic and thalamocortical
networks. J Neurosci 1996b; 16: 2788-808.
45. Timofeev I, Steriade M. Low-frequency rhythms in the thalamus of
intact-cortex and decorticated cats. J Neurophysiol 1996; 76: 4152-68.
46. Timofeev I, Contreras D, Steriade M. Synaptic responsiveness of cortical
and thalamic neurones during various phases of slow sleep oscillation
in cat. J Physiol Lond 1996; 494: 265-78.
47. Villablanca J. Role of the thalamus in sleep control: sleep-wakefulness
studies in chronic diencephalic and athalamic cats. In: O Petre-Quadens,
JD Schlag, eds. Basic Sleep Mechanisms. New York: Academic Press, 1974,
pp. 51-81.
48. Wilson MA, McNaughton BL. Reactivation of hippocampal ensemble memories
during sleep. Science 1994; 265: 676-9.
This work was supported by grants from the Medical Research Council of
Canada and Human Frontier Science Program. F. Amzica is a postdoctoral
fellow, partially supported by Fonds de Recherche en Santé du Québec.
We thank D. Contreras and I. Timofeev for their collaboration in some
unpublished experiments.
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