Search PubMed⌕ Search

Biomedical subjects

M Steriade

Publications and source records attributed to M Steriade.

At least 73 records · Page 4Linked to original sources
PubMed1997

Synchronization of low-frequency rhythms in corticothalamic networks.

We have investigated the degree of synchronization between cortical, thalamic reticular and thalamocortical neurons of cats during low-frequency (< 15 Hz) sleep-like oscillations, as they appear under anaesthesia. We have also studied the effects exerted by cortical stimulation on the synchronization among thalamic units. Parallel experiments [Steriade et al. (1996) J. Neurosci. 16, 392-417] in this laboratory have demonstrated the similarity between the slow oscillation (< 1 Hz) under ketamine-xylazine anaesthesia and that occurring during the natural state of resting sleep. Spontaneous activity was recorded simultaneously, with independent microelectrodes, from groups of two to five physiologically identified neurons. The rhythmicity of spontaneous activity and the temporal relations between cellular discharges were statistically evaluated by auto- and crosscorrelation techniques. We have found no topography in the distribution of synchronization between thalamic reticular and thalamocortical cells. Only the slow, cortical-generated oscillation (< 1 Hz) displayed a stable frequency and correlation among groups of cortical and thalamic cells. The other two sleep oscillations (thalamic-generated spindles at 7-14 Hz and clock-like delta at 1-4 Hz) fluctuated in frequency and the degree of correlation between neurons varied. Cortical volleys entrained and synchronized thalamic cells, and triggered synchronized spindling in the thalamus. These results extend for large populations of cortical and thalamic neurons the phase relations found in intracellular recordings.

Animals↗
PubMed1997

Spindle oscillations during cortical spreading depression in naturally sleeping cats.

Spindling activity characterizes the EEG of animals and humans in the early stages of resting sleep. Spindles are defined as waxing and waning rhythmic waves at 7-14 Hz that recur periodically every 3-10 s. Spindling originates in the thalamus, but a role for the cerebral cortex in triggering and synchronizing thalamic spindles was shown by stimulation of the contralateral cortex avoiding antidromic activation of thalamocortical axons and by diminished coherency of thalamic spindles after hemidecortication. Spontaneous spindles under barbiturate anesthesia are waxing and waning but under ketamine-xylazine anesthesia or when evoked by strong stimuli spindle waves are almost exclusively waning, i.e. they start with maximum amplitude and then decrease progressively. Waxing and waning of spindles has been ascribed to progressive entrainment of units into the oscillation followed by a progressive desynchronization. Therefore, exclusively waning spindles would be produced by an initial high synchrony in the corticothalamic network. Such a situation is observable upon strong stimulation or, spontaneously, when spindles are paced by the slow cortical oscillation and preceded by a strong corticothalamic drive. We have conducted experiments in naturally sleeping cats to verify the occurrence of two patterns of spindle oscillations and to test the role of the cortex in synchronizing and shaping spindles. We have found that indeed two types of spindles (waxing and waning or mostly waning) occur in naturally sleeping animals. We also demonstrate that during cortical spreading depression spindles are less synchronous and only of the waxing and waning type. As cortical activity recovers, waning spindles reappear and are preceded by electroencephalogram deflections which are related to corticothalamic depolarizing inputs. Our results strongly support the hypothesis of the role of the cerebral cortex in shaping and synchronizing thalamically generated spindles.

Animals↗
PubMed1997

Synchronized activities of coupled oscillators in the cerebral cortex and thalamus at different levels of vigilance.

The cerebral cortex and thalamus constitute a unified oscillatory machine displaying different spontaneous rhythms that are dependent on the behavioral state of vigilance. In vivo multi-site recordings from a variety of neocortical areas and related thalamic nuclei in cat, including dual simultaneous intracellular recordings, demonstrate that corticofugal volleys are effective in synchronizing fast (20-50 Hz) and low-frequency (< 15 Hz) oscillations in thalamocortical networks, characterizing activated and de-afferented states. (i) Fast spontaneous oscillations depend on the depolarization of thalamic and cortical cells and appear in a sustained manner during waking and REM sleep. Corticothalamic neurons, discharging high-frequency (400 Hz) spike-bursts at 30-40 Hz, are good candidates to synchronize fast oscillations in reentrant thalamocortical loops. Weakly synchronized, fast spontaneous oscillations may be reset and become robustly coherent after relevant sensory stimuli in waking or internal signals during the dreaming state. (ii) During quiescent sleep, the long-range synchronization of brain electrical activity results from synchronous hyperpolarizations in forebrain neurons. The corticothalamic inputs during the depolarizing component of the slow oscillation (< 1 Hz) are effective in grouping the thalamic-generated sleep rhythms (spindles at 7-14 Hz and delta at 1-4 Hz) into complex wave-sequences. These inputs also control the shape of spindles, and favor the long-range synchronization and nearly simultaneous appearance of spindles. (iii) The cortical control of thalamic activity is also demonstrated in spike-wave-seizures developing from sleep patterns. More than half of thalamocortical neurons are silent during spike-wave seizures, being tonically hyperpolarized, and display IPSPs (closely related to the paroxysmal depolarizing shifts of cortical cells) that are determined by the pattern of activities in thalamic reticular cells. All these data congruently show the power of cortical control upon thalamic oscillators.

Animals↗
PubMed1997

Plateau potentials in cat neocortical association cells in vivo: synaptic control of dendritic excitability.

The dendrites of neocortical pyramidal cells are bombarded by myriads of synaptic inputs and express active conductances generating prominent plateau potentials. We have examined in vivo the possibility that spontaneous synaptic inputs trigger or terminate plateau potentials after blockage of K+ currents. Under barbiturate anaesthesia, pairs of cortical cells were intracellularly recorded with sharp electrodes from the cat's association cortex (areas 5-7). In one pyramidal cell, K+ channels were blocked with intracellular Cs+, while in the simultaneously impaled pyramidal cell the K+ conductances were left intact to act as a control; this second cell allowed recognition of spontaneous spindle-related synaptic activity. Depolarizing current pulses elicited single, all-or-none plateau potentials (60-70 mV, 0.1-0.4 s). Plateau potentials slowly repolarized towards a break point of fast repolarization around -20 mV. Thalamic-evoked inhibitory postsynaptic potentials consistently shut off the plateaus. Synchronized spontaneous activity, as occurring during thalamic-generated spindle oscillations, either triggered or blocked the plateaus. These results suggest that spontaneously occurring synaptic activation during synchronized oscillatory states, such as those that occur during sleep spindles in vivo, may exert a strong control over the dendritic excitability in neocortical pyramidal cells.

Action Potentials↗
PubMed1997

Dynamic interactions determine partial thalamic quiescence in a computer network model of spike-and-wave seizures.

In vivo intracellular recording from cat thalamus and cortex was performed during spontaneous spike-wave seizures characterized by synchronously firing cortical neurons correlated with the electroencephalogram. During these seizures, thalamic reticular (RE) neurons discharged with long spike bursts riding on a depolarization, whereas thalamocortical (TC) neurons were either entrained into the seizures (40%) or were quiescent (60%). During quiescence, TC neurons showed phasic inhibitory postsynaptic potentials (IPSPs) that coincided with paroxysmal depolarizing shifts in the simultaneously recorded cortical neuron. Computer simulations of a reciprocally connected TC-RE pair showed two major modes of TC-RE interaction. In one mode, a mutual oscillation involved direct TC neuron excitation of the RE neuron leading to a burst that fed back an IPSP into the TC neuron, producing a low-threshold spike. In the other, quiescent mode, the TC neuron was subject to stronger coalescing IPSPs. Simulated cortical stimulation could trigger a transition between the two modes. This transition could go in either direction and was dependent on the precise timing of the input. The transition did not always follow the stimulation immediately. A larger, multicolumnar simulation was set up to assess the role of the TC-RE pair in the context of extensive divergence and convergence. The amount of TC neuron spiking generally correlated with the strength of total inhibitory input, but large variations in the amount of spiking could be seen. Evidence for mutual oscillation could be demonstrated by comparing TC neuron firing with that in reciprocally connected RE neurons. An additional mechanism for TC neuron quiescence was assessed with the use of a cooperative model of gamma-aminobutyric acid-B (GABA(B))-mediated responses. With this model, RE neurons receiving repeated strong excitatory input produced TC neuron quiescence due to burst-duration-associated augmentation of GABA(B) current. We predict the existence of spatial inhomogeneity in apparently generalized spike-wave seizures, involving a center-surround pattern. In the center, intense cortical and RE neuron activity would be associated with TC neuron quiescence. In the surround, less intense hyperpolarization of TC neurons would allow low-threshold spikes to occur. This surround, an "epileptic penumbra," would be the forefront of the expanding epileptic wave during the process of initial seizure generalization. Therapeutically, we would then predict that agents that reduce TC neuron activity would have a greater effect on seizure onset than on ongoing spike-wave seizures or other thalamic oscillations.

Action Potentials↗
PubMed1997

Intracellular and computational characterization of the intracortical inhibitory control of synchronized thalamic inputs in vivo.

We investigated the presence and role of local inhibitory cortical control over synchronized thalamic inputs during spindle oscillations (7-14 Hz) by combining intracellular recordings of pyramidal cells in barbiturate-anesthetized cats and computational models. The recordings showed that 1) similar excitatory postsynaptic potential (EPSP)/inhibitory postsynaptic potential (IPSP) sequences occurred either during spindles or following thalamic stimulation; 2) reversed IPSPs with chloride-filled pipettes transformed spindle-related EPSP/IPSP sequences into robust bursts with spike inactivation, resembling paroxysmal depolarizing shifts during seizures; and 3) dual simultaneous impalements showed that inhibition associated with synchronized thalamic inputs is local. Computational models were based on reconstructed pyramidal cells constrained by recordings from the same cells. These models showed that the transformation of EPSP/IPSP sequences into fully developed spike bursts critically needs a relatively high density of inhibitory currents in the soma and proximal dendrites. In addition, models predict significant Ca2+ transients in dendrites due to synchronized thalamic inputs. We conclude that synchronized thalamic inputs are subject to strong inhibitory control within the cortex and propose that 1) local impairment of inhibition contributes to the transformation of spindles into spike-wave-type discharges, and 2) spindle-related inputs trigger Ca2+ events in cortical dendrites that may subserve plasticity phenomena during sleep.

Animals↗
PubMed1997

Absence of a prevalent laminar distribution of IPSPs in association cortical neurons of cat.

Absence of a prevalent laminar distribution of IPSPs in association cortical neurons of cat. J. Neurophysiol. 78: 2742-2753, 1997. The depth distribution of inhibitory postsynaptic potentials (IPSPs) was studied in cat suprasylvian (association) cortex in vivo. Single and dual simultaneous intracellular recordings from cortical neurons were performed in the anterior part of suprasylvian gyrus (area 5). Synaptic responses were obtained by stimulating the suprasylvian cortex, 2-3 mm anterior to the recording site, as well as the thalamic lateral posterior (LP) nucleus. Neurons were recorded from layers 2 to 6 and were classified as regular spiking (RS, n = 132), intrinsically bursting (IB, n = 24), and fast spiking (FS, n = 4). Most IB cells were located in deep layers (below 0.7 mm, n = 19), but we also found some IB cells more superficially (between 0.2 and 0.5 mm, n = 5). Deeply lying corticothalamic neurons were identified by their antidromic invasion on thalamic stimulation. Neurons responded with a combination of excitatory postsynaptic potentials (EPSPs) and IPSPs to both cortical and thalamic stimulation. No consistent relation was found between cell type or cell depth and the amplitude or duration of the IPSPs. In response to thalamic stimulation, RS cells had IPSPs of 7.9 +/- 0.9 (SE) mV amplitude and 88.9 +/- 6.4 ms duration. In IB cells, IPSPs elicited by thalamic stimulation had 7.4 +/- 1.3 mV amplitude and 84.7 +/- 14.3 ms duration. The differences between the two (RS and IB) groups were not statistically significant. Compared with thalamically elicited inhibitory responses, cortical stimulation evoked IPSPs with higher amplitude (12.3 +/- 1.7 mV) and longer duration (117 +/- 17.3 ms) at all depths. Both cortically and thalamically evoked IPSPs were predominantly monophasic. Injections of Cl- fully reversed thalamically as well as cortically evoked IPSPs and revealed additional late synaptic components in response to cortical stimulation. These data show that the amount of feed forward and feedback inhibition to cat's cortical association cells is not orderly distributed to distinct layers. Thus local cortical microcircuitry goes beyond the simplified structure determined by cortical layers.

Animals↗
PubMed1997

The K-complex: its slow (<1-Hz) rhythmicity and relation to delta waves.

The K-complex is a major graphoelement of sleep EEG. This report demonstrates that K-complexes emerge from a cortically generated slow (<1-Hz) oscillation. Human EEG as well as cat cellular and field potential recordings converge into demonstrating that the K-complex results from a synchronized cortical network that imposes periodic excitatory and inhibitory actions on cortical neurons. We additionally show the correspondence between neuronal activities and the shape of the K-complex. Spectral analysis confirms the periodic recurrence of human K-complexes, with main peaks at 0.5 to 0.7 Hz. It is also shown that the spectral content in the delta band (1 to 4 Hz) is partially due to the shape and duration of the K-complex.

Action Potentials↗
PubMed1996

Control of spatiotemporal coherence of a thalamic oscillation by corticothalamic feedback.

The mammalian thalamus is the gateway to the cortex for most sensory modalities. Nearly all thalamic nuclei also receive massive feedback projections from the cortical region to which they project. In this study, the spatiotemporal properties of synchronized thalamic spindle oscillations (7 to 14 hertz) were investigated in barbiturate-anesthetized cats, before and after removal of the cortex. After complete ipsilateral decortication, the long-range synchronization of thalamic spindles in the intact cortex hemisphere changed into disorganized patterns with low spatiotemporal coherence. Local thalamic synchrony was still present, as demonstrated by dual intracellular recordings from nearby neurons. In the cortex, synchrony was insensitive to the disruption of horizontal intracortical connections. These results indicate that the global coherence of thalamic oscillations is determined by corticothalamic projections.

Anesthesia↗
PubMed1996

Mechanisms of long-lasting hyperpolarizations underlying slow sleep oscillations in cat corticothalamic networks.

1. To explore the nature of the long-lasting hyperpolarizations that characterize slow oscillations in corticothalamic circuits in vivo, intracellular recordings were obtained under ketamine-xylazine anaesthesia from cortical (Cx) cells of the cat precruciate motor cortex, thalamic reticular (RE) cells from the rostrolateral sector, and thalamocortical (TC) cells from the ventrolateral (VL) nucleus. 2. Measurements in the three cell types showed input resistance (Rin) to be highest during the long-lasting hyperpolarizations that correspond to depth-positive waves of the cortical EEG. Rin was lowest during the early phase of high-amplitude depth-negative EEG waves and increased thereafter until the next cycle of the slow oscillation. 3. Spontaneous long-lasting hyperpolarizations were compared with those evoked by dorsal thalamic stimulation. Voltage versus current (V-I) plots showed similar membrane potential (Vm) ranges and slopes for spontaneous and evoked hyperpolarizations in both Cx and RE cells. V-I plots from TC cells had similar slopes, but Vm during evoked hyperpolarizations was displaced towards more negative values. 4. Intracellular injection of constant hyperpolarizing current in Cx cells increased the amplitude of the initial part of the depolarizing plateau of the slow oscillation, but decreased the amplitude of the last part. 5. These results suggest disfacilitation to be the dominant mechanism in the membrane of cortical and thalamic cells during the spontaneous long-lasting hyperpolarizations, which shape and synchronize slow oscillations in corticothalamic networks. In Cx and RE cells, the same mechanism underlies thalamically evoked long-lasting hyperpolarizations. By contrast, evoked responses in TC cells show a strong additional hyperpolarizing factor. We propose that GABAB processes are stronger in TC than in Cx neurones, thus rendering the thalamus an easier target for absence-type epileptic phenomena through potentiation of thalamic rebound capabilities.

Animals↗
PubMed1996

Synaptic responsiveness of cortical and thalamic neurones during various phases of slow sleep oscillation in cat.

1. The fluctuations during various phases of the slow sleep oscillation (< 1 Hz) in synaptic responsiveness of motor cortical (Cx), thalamic reticular (RE) and thalamocortical (TC) neurones were investigated intracellularly in cats under ketamine-xylazine anaesthesia. Orthodromic responses to stimuli applied to brachium conjunctivum (BC) axons and corticothalamic pathways were studied. The phases of slow oscillation consist of a long-hyperpolarized, followed by a sharp depth-negative EEG deflection and a series of faster waves that are associated with the depolarization of Cx and RE neurones, while TC cells display a sequence of IPSPs within the spindle frequency. 2. BC-evoked bisynaptic excitatory postsynaptic potentials (EPSPs) in Cx and RE neurones were drastically reduced in amplitude during the long-lasting hyperpolarization and the early part of the depolarizing phase. By contrast, the BC-evoked monosynaptic EPSPs of TC cells were not diminished during the depth-positive EEG wave, but the hyperpolarization during this phase of the slow oscillation prevented TC neurones transferring prethalamic signals to the cortex. 3. At variance with the diminished bisynaptic EPSPs evoked in response to BC stimuli during the long-lasting hyperpolarization, Cx-evoked monosynaptic EPSPs in Cx cells increased linearly with hyperpolarization during this phase of the slow oscillation. Similarly, the amplitudes of Cx-evoked EPSPs in RE and TC cells were not diminished during the long-lasting hyperpolarization. 4. The diminished responsiveness of Cx and RE neurones to prethalamic volleys during the long-lasting hyperpolarization is attributed to gating processes at the level of TC cells that, because of their hyperpolarization, do not transfer prethalamic information to further relays.

Animals↗
PubMed1996

Synchronization of fast (30-40 Hz) spontaneous oscillations in intrathalamic and thalamocortical networks.

The synchronization of fast (mainly 30 to 40 Hz) oscillations in intrathalamic and thalamocortical (TC) networks of cat was studied under ketamine-xylazine anesthesia and in behaving animals by means of field potential, extra- and intracellular recordings from multiple sites in the thalamic reticular (RE) nucleus, dorsal (sensory, motor, and intralaminar) thalamic nuclei, and related neocortical areas. Far from being restricted to tonically activated behavioral states, the fast oscillations also appeared during resting sleep and deep anesthesia, when they occurred over the depolarizing component of the slow (<1 Hz) oscillation and were suppressed during the prolonged hyper-polarizations of RE, TC, and cortical neurons. The synchronization of fast rhythms among different thalamic foci was robust. Fast rhythmic cortical waves and subthreshold depolarizing potentials in TC neurons were highly coherent; however, the synchronization of the fast oscillation required recordings from reciprocally related neocortical and thalamic foci, as identified by monosynaptic responses in both directions. The short-range spatial confinement of coherent fast rhythms contrasted with the large-scale synchronization of low-frequency sleep rhythms. Transient fast rhythms, appearing over the depolarizing envelope of the slow sleep oscillation, became sustained when brain activation was elicited by stimulation of mesopontine cholinergic nuclei or during brain-active behavioral states in chronic experiments. These data demonstrate that fast rhythms are part of the background electrical activity of the brain and that desynchronization, used to designate brain-active states, is an erroneous term inasmuch as the fast oscillations are synchronized not only in intracortical but also in intrathalamic and TC networks.

Action Potentials↗
PubMed1996

Intracortical and corticothalamic coherency of fast spontaneous oscillations.

We report that fast (mainly 30- to 40-Hz) coherent electric field oscillations appear spontaneously during brain activation, as expressed by electroencephalogram (EEG) rhythms, and they outlast the stimulation of mesopontine cholinergic nuclei in acutely prepared cats. The fast oscillations also appear during the sleep-like EEG patterns of ketamine/xylazine anesthesia, but they are selectively suppressed during the prolonged phase of the slow (<1-Hz) sleep oscillation that is associated with hyperpolarization of cortical neurons. The fast (30- to 40-Hz) rhythms are synchronized intracortically within vertical columns, among closely located cortical foci, and through reciprocal corticothalamic networks. The fast oscillations do not reverse throughout the depth of the cortex. This aspect stands in contrast with the conventional depth profile of evoked potentials and slow sleep oscillations that display opposite polarity at the surface and midlayers. Current-source-density analyses reveal that the fast oscillations are associated with alternating microsinks and microsources across the cortex, while the evoked potentials and the slow oscillation display a massive current sink in midlayers, confined by two sources in superficial and deep layers. The synchronization of fast rhythms and their high amplitudes indicate that the term "EEG desynchronization," used to designate brain-aroused states, is incorrect and should be replaced with the original term, "EEG activation" [Moruzzi, G. & Magoun, H.W. (1949) Electroencephalogr. Clin. Neurophysiol. 1, 455-473].

Action Potentials↗
PubMed1996

Spindle oscillation in cats: the role of corticothalamic feedback in a thalamically generated rhythm.

1. Spindles represent an oscillatory activity (7-14 Hz) of the electroencephalogram (EEG) originating in the thalamus and appearing during early stages of sleep. We investigated: (i) the phase relations between thalamic and cortical neurons during this rhythm; (ii) the patterns of spindles under different anaesthetics and their modifications at various levels of the membrane potential (Vm); and (iii) the potentiating role of the corticothalamic feedback in the genesis of spindles. Intra- and extracellular recordings were performed in cats from reticular and dorsal thalamic nuclei, as well as from various cortical areas. 2. In thalamic reticular neurons, spindles were sequences of waves at 7-14 Hz, riding on a prolonged depolarizing plateau and occurring in phase with depth-negative cortical EEG waves. In thalamocortical cells, spindles consisted of inhibitory postsynaptic potentials (IPSPs) in phase with depth-positive cortical EEG waves and occasionally leading to rebound spike bursts. In cortical cells, spindle waves were rhythmic (7-14 Hz) excitatory postsynaptic potentials (EPSPs) that sometimes gave rise to action potentials. Spindles occurred in phase among thalamic reticular, thalamocortical and neocortical neurons. 3. In thalamic reticular neurons, spindle waves and their depolarizing plateaux increased in amplitude with slight cellular hyperpolarization, but at a Vm more negative than -80 or -85 mV they decreased in amplitude. No frequency alterations were observed with these Vm changes. 4. The waxing-and-waning pattern of spontaneous spindles under barbiturate anaesthesia was distinct from the waning pattern under ketamine-xylazine anaesthesia. Under all anaesthetics, spindles had a waning pattern when elicited by cortical stimuli. The amplitude of cortical-evoked spindle waves diminished with the decrease in stimulation intensity. 5. Under urethane or ketamine-xylazine anaesthesia, spindle sequences were grouped by a cortically generated slow oscillation (< 1 Hz) and were preceded by a depth-positive EEG wave that corresponded to a prolonged hyperpolarization in all three investigated (cortical, thalamic reticular, and thalamocortical) cellular types. 6. We propose that the waxing pattern of spindle oscillation is due to a progressive entrainment of units into the oscillation until a maximum number is reached, depending on the background activity in the network. The phase relations between cortical, thalamic reticular and thalamocortical neurons are ascribed to distributed excitatory signals from thalamocortical neurons to both cortical and reticular neurons at each cycle of the oscillation. In turn, cortical neurons provide a powerful drive to potentiate the genesis of thalamic spindles.

Animals↗
PubMed1996

Progressive cortical synchronization of ponto-geniculo-occipital potentials during rapid eye movement sleep.

Phasic events, termed ponto-geniculo-occipital potentials, appear in the brainstem, thalamus and cerebral cortex during rapid eye movement sleep. In the cat, the species of choice for ponto-geniculo-occipital studies, these field potentials are usually recorded from the lateral geniculate thalamic nucleus and visual cortex. However, the fact that brainstem cholinergic neurons play a crucial role in the transfer of ponto-geniculo-occipital potentials to the thalamus, coupled with the evidence that mesopontine tegmental neurons project to virtually all thalamic nuclei, together explain why ponto-geniculo-occipital potentials are recorded over widespread territories, beyond the visual thalamocortical system. Here we demonstrate, by means of multi-site unit and field potential recordings from sensory, motor and association cortical areas in behaving cats, that: (i) ponto-geniculo-occipital potentials appear synchronously over the neocortex; and (ii) that their cortical synchronization develops progressively from the period preceding rapid eye movement sleep by 30-90 s (pre-rapid eye movement), to reach the highest degree of intracortical coherence during later epochs of rapid eye movement sleep. We propose that the widespread coherence of cortical ponto-geniculo-occipital potentials underlies the synchronization of fast oscillations (30-40 Hz) during rapid eye movement sleep over many, functionally distinct cortical territories implicated in dreaming, as brainstem-induced ponto-geniculo-occipital-like potentials are consistently followed by such fast oscillations.

Animals↗
PubMed1996

Low-frequency rhythms in the thalamus of intact-cortex and decorticated cats.

1. The patterns and synchronization of low-frequency, sleeplike rhythms (slow, spindle and delta oscillations) were compared in the intact-cortex and decorticated hemispheres of cats under ketamine-xylazine anesthesia. Intracellular recordings were performed in intact and decorticated hemispheres from 58 rostrolateral thalamic reticular (RE) neurons and from 164 thalamocortical (TC) neurons in the ventrolateral (VL) nucleus. In the decorticated hemisphere, dual intracellular recordings were performed from five RE-VL cell couples and from 12 TC cell couples within the VL nucleus. In addition, field potentials were simultaneously recorded from the neocortex (electroencephalogram) and ipsilateral thalamus [electrothalamogram (EThG)] of the intact (right) hemisphere, while EThG was recorded from the VL nucleus of the decorticated (left) hemisphere. 2. The slow oscillation (< 1 Hz) was absent in all 72 VL cells and in 23 of 25 RE cells from the decorticated hemisphere, as well as in the EThG recorded from the VL nucleus in the decorticated hemisphere, whereas it was simultaneously present in the cortex and thalamus of the intact hemisphere. The remaining two RE neurons (8%) in the decorticated hemisphere oscillated in close time relation with the slow oscillation in the cortex and thalamus of the opposite hemisphere; averaged activities showed that the onset of depolarization in RE cell followed 12 ms after the sharp depth-negative (depolarizing) component in the contralateral cortex. We view this result as the electrophysiological correlate of a disynaptic excitatory pathway consisting of crossed cortical projections, first relayed in contralateral dorsal thalamic nuclei. 3. The patterns of thalamic spindles (7-14 Hz) differed between the two hemispheres. Whereas the decorticated hemisphere displayed prolonged, waxing and waning spindles, the spindles in the intact-cortex hemisphere were short and exclusively waning and followed the depth-negative component of cortical slow oscillation. This result indicates that the synchronized corticothalamic drive associated with the slow oscillation fully entrains thalamic circuits from the onset of spindles, thus preventing further waxing. Similar differences between waxing and waning and waning spindles were obtained by stimulating with different intensities the thalamus in the decorticated hemisphere. 4. Simultaneous intracellular recordings from two VL cells or from RE and VL cells showed nearly simultaneous spindle sequences in the decorticated hemisphere. 5. The hyperpolarization-activated intrinsic delta oscillation (1-4 Hz) of TC cells was asynchronous in the decorticated hemisphere. 6. These results strengthen the idea that the slow oscillation is cortical in origin; demonstrate a full, short-range, intrathalamic synchrony of spindles in the absence of cortex; and indicate that the pattern of spindles, a sleep rhythm that is conventionally regarded as purely thalamic, is shaped by the corticothalamic feedback.

Animals↗