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M Steriade

Publications and source records attributed to M Steriade.

At least 109 records · Page 6Linked to original sources
PubMed1993

Electrophysiological properties of intralaminar thalamocortical cells discharging rhythmic (approximately 40 HZ) spike-bursts at approximately 1000 HZ during waking and rapid eye movement sleep.

Thalamocortical neurons located in the large-celled district of the cat intralaminar centrolateral nucleus were found to discharge spike-bursts with unusually high frequencies (800-1000 Hz) during spindle oscillations of the electroencephalogram. In chronically implanted animals, similar spike-bursts were also fired during wakefulness and rapid eye movement sleep, two behavioral states in which other thalamocortical neurons tonically fire single spikes. Such high-frequency spike-bursts recurred with a fast rhythm of 20-40 Hz during waking and rapid eye movement sleep. Intracellular recordings under barbiturate anesthesia showed that, during spindle oscillations, the spike-bursts of intralaminar neurons are generated by brief low-threshold spikes with a much shorter refractory phase than in other thalamocortical cells. Depolarizing pulses from the resting membrane potential triggered fast oscillations (20-80 Hz) crowned by short high-frequency (800-1000 Hz) spike-bursts. During the inter-spindle epochs, the "tonic" firing of these neurons was, in fact, a fast oscillation (30-40 Hz) of the membrane potential leading to single spikes or spike-doublets. Autocorrelograms computed from inter-spindle epochs, at relatively depolarized levels, confirmed the presence of multiple peaks at this fast rhythm. The properties of these neurons make them well suited for the distribution of fast rhythms during arousal and rapid eye movement sleep over the cerebral cortex.

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PubMed1993

Central core modulation of spontaneous oscillations and sensory transmission in thalamocortical systems.

Central core (brainstem, diencephalic and basal forebrain) systems influence the functional modes of thalamic and cortical neurons during behavioral states of vigilance. Recent studies in vivo and in vitro have focused on the cellular properties of central core systems and their modulation of slow sleep oscillations, fast rhythms during arousal and dreaming state, and the fine inhibitory sculpturing of afferent signals.

Animals↗
PubMed1993

Electrophysiological properties of cat reticular thalamic neurones in vivo.

1. The electrophysiological properties of neurones of the reticular thalamic (RE) nucleus were studied in acutely prepared cats under urethane anaesthesia. 2. Two main types of neuronal firing were recorded. At the resting membrane potential (-60 to -65 mV) tonic repetitive firing was elicited when the cell was activated synaptically or by current injection. From membrane potentials more negative than -75 mV, synaptic or direct stimulation generated a burst of action potentials. 3. The burst of RE cells consisted of a discharge of four to eight spikes riding on a slowly growing and decaying depolarization. The discharge rate during the burst showed a characteristic increase, followed by a decrease in frequency. 4. The burst response behaved as a graded phenomenon, as its magnitude was modulated by changing the intensity of the synaptic volley or the intensity of the injected current. 5. Spike-like small potentials presumably of dendritic origin occurred spontaneously and were triggered by synaptic or direct stimulation. They were all-or-none, voltage-dependent events. We postulate that these spikes originate in several hot spots in the dendritic arbor, with no reciprocal refractoriness and may generate multi-component depolarizations at the somatic level. 6. Excitatory postsynaptic potentials (EPSPs) evoked by internal capsule stimulation consisted of two components, the late one being blocked by hyperpolarization. Such compound EPSPs were followed by a period of decreased excitability during which a second response was diminished in amplitude. 7. A series of depolarizing waves at the frequency range of spindle oscillations was triggered by internal capsule stimulation. The individual depolarizing waves constituting the spindle oscillation gradually decreased in amplitude when decreasing the intensity of the stimulation. 8. These results, showing that RE cells are endowed with an excitable dendritic tree and a graded bursting behaviour, support the proposed role of RE nucleus as the generator and synchronizer of spindle rhythmicity.

Animals↗
PubMed1993

Electrophysiology of cat association cortical cells in vivo: intrinsic properties and synaptic responses.

1. The intrinsic properties and synaptic responses of association cortical neurons (n = 179) recorded from cat's areas 5 and 7 were studied in vivo. Intracellular recordings were performed under urethane anesthesia. Resting membrane potential (Vm) was -71.7 +/- 1.2 (SE) mV, amplitude of action potential was 83.7 +/- 2.3 mV, and input resistance was 18.4 +/- 1.8 M omega. Cells were identified ortho- and antidromically from lateroposterior and centrolateral thalamic nuclei and from homotopic foci in the contralateral cortex. Physiologically identified neurons were intracellularly stained with Lucifer yellow (LY) and found to be pyramidal-shaped elements (n = 21). 2. We classified the neurons as regular-spiking and intrinsically bursting cells. Regular-spiking cells were further classified as slow- and fast-adapting according to the adaptation of spike frequency during long-lasting depolarizing current pulses. 3. Regular-spiking, slow-adapting neurons had a monophasic afterhyperpolarization (AHP) or a biphasic AHP with fast and medium components (FAHP, mAHP). Slow-adapting behavior was observed in 84% (n = 119) of the regular-spiking cells. 4. Regular-spiking, fast-adapting cells only fired a train of spikes at the beginning of the pulse. Thereafter, the Vm remained as a depolarizing plateau, occasionally triggering some spikes. These neurons had a monophasic AHP and represented 16% (n = 23) of the regular-spiking neurons. 5. Intrinsically bursting neurons (n = 37) were observed in 20% of neocortical cells at depolarized Vm. Their action potential was followed by a marked depolarizing afterpotential (DAP). Rhythmic (4-10 Hz) bursts occurred during long-lasting depolarizing current pulses. 6. Small (3-10 mV), fast (1.5-4 ms), all-or-none depolarizing potentials were triggered by depolarizing current pulses. They are tentatively regarded as dendritic spikes recorded from the soma because their rate of occurrence changed as a function of the Vm and they were eventually blocked by hyperpolarization. 7. Synaptic stimulation of either thalamic or homotopic contralateral cortical areas elicited a sequence of excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs). Two components of the EPSP were revealed. At a hyperpolarized Vm, the initial component of the EPSP increased in amplitude, whereas the secondary component was blocked. Repetitive (10 Hz) stimulation of the thalamus or contralateral cortex elicited incremental responses. The augmentation phenomenon was due to an increase in the secondary component of the EPSP. The cortically elicited augmenting responses survived extensive thalamic lesions. A short IPSP and a long-lasting IPSP were evoked by thalamic or cortical stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1993

Cholinergic and noradrenergic modulation of the slow (approximately 0.3 Hz) oscillation in neocortical cells.

1. The pedunculopontine tegmental (PPT) cholinergic nucleus and the locus coeruleus (LC) noradrenergic nucleus were electrically stimulated to investigate their effects on the recently described slow oscillation (approximately 0.3 Hz) of neocortical neurons. Intracellular recordings of slowly oscillating, regular-spiking and intrinsically bursting neurons from cortical association areas 5 and 7 (n = 140) were performed in anesthetized cats. 2. Pulse trains to the PPT nucleus produced the blockage of rhythmic (approximately 0.3 Hz) depolarizing-hyperpolarizing sequences in 79% of tested cortical neurons and transformed this slow cellular rhythm into tonic firing. The latency of the cortical cellular response to PPT stimulation was 1.2 +/- 0.5 (SE) s and its duration was 15.9 +/- 1.9 s. The PPT-elicited suppression of the slow cellular oscillation was accompanied by an activation of the electroencephalogram (EEG) having a similar time course. Fast Fourier transform analyses of EEG activities before and after PPT stimulation showed that the PPT-evoked changes consisted of decreased power of slow rhythms (0-8 Hz) and increased power of fast rhythms (24-33 Hz); these changes were statistically significant. 3. The blockage of the slow cellular oscillation was mainly achieved through the diminution or suppression of the long-lasting hyperpolarizations separating the rhythmic depolarizing envelopes. This effect was observed even when PPT pulse trains disrupted the oscillation without inducing overt depolarization and increased firing rate. The durations of the prolonged hyperpolarizations were measured during a 40-s window (20 s before and 20 s after the PPT pulse train) and were found to decrease from 1.5 +/- 0.2 to 0.7 +/- 0.1 s. The values of the product resulting from the duration (in seconds), the amplitude (in millivolts), and number of such hyperpolarizing events within 20-s periods were 51.5 +/- 5 and 5.1 +/- 1.9 before and after PPT stimulation, respectively. 4. The PPT effect was suppressed by systemic administration of a muscarinic antagonist, scopolamine, but not by mecamylamine, a nicotinic antagonist. 5. The PPT effect on cellular and EEG cortical slow oscillation survived, although its duration was reduced, in animals with kainate-induced lesions of thalamic nuclei projecting to areas 5 and 7 (n = 3) as well as in animals with similar excitotoxic lesions leading to extensive neuronal loss in nucleus basalis (n = 2). These data indicate that the PPT effect is transmitted to neocortex through either thalamic or basal forebrain relays.(ABSTRACT TRUNCATED AT 400 WORDS)

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PubMed1993

A novel slow (< 1 Hz) oscillation of neocortical neurons in vivo: depolarizing and hyperpolarizing components.

We describe a novel slow oscillation in intracellular recordings from cortical association areas 5 and 7, motor areas 4 and 6, and visual areas 17 and 18 of cats under various anesthetics. The recorded neurons (n = 254) were antidromically and orthodromically identified as corticothalamic or callosal elements receiving projections from appropriate thalamic nuclei as well as from homotopic foci in the contralateral cortex. Two major types of cells were recorded: regular-spiking (mainly slow-adapting, but also fast-adapting) neurons and intrinsically bursting cells. A group of slowly oscillating neurons (n = 21) were intracellularly stained and found to be pyramidal-shaped cells in layers III-VI, with luxuriant basal dendritic arbors. The slow rhythm appeared in 88% of recorded neurons. It consisted of slow depolarizing envelopes (lasting for 0.8-1.5 sec) with superimposed full action potentials or presumed dendritic spikes, followed by long-lasting hyperpolarizations. Such sequences recurred rhythmically at less than 1 Hz, with a prevailing oscillation between 0.3 and 0.4 Hz in 67% of urethane-anesthetized animals. While in most neurons (approximately 70%) the repetitive spikes superimposed on the slow depolarization were completely blocked by slight DC hyperpolarization, 30% of cells were found to display relatively small (3-12 mV), rapid, all-or-none potentials after obliteration of full action potentials. These fast spikes were suppressed in an all-or-none fashion at Vm more negative than -90 mV. The depolarizing envelope of the slow rhythm was reduced or suppressed at a Vm of -90 to -100 mV and its duration was greatly reduced by administration of the NMDA blocker ketamine. In keeping with this action, most (56%) neurons recorded in animals under ketamine and nitrous oxide or ketamine and xylazine anesthesia displayed the slow oscillation at higher frequencies (0.6-1 Hz) than under urethane anesthesia (0.3-0.4 Hz). In 18% of the oscillating cells, the slow rhythm mainly consisted of repetitive (15-30 Hz), relatively short-lasting (15-25 msec) IPSPs that could be revealed by bringing the Vm at more positive values than -70 mV. The long-lasting (approximately 1 sec) hyperpolarizing phase of the slow oscillation was best observed at the resting Vm and was reduced at about -100 mV. Simultaneous recording of another cell across the membrane demonstrated synchronous inhibitory periods in both neurons. Intracellular diffusion of Cl- or Cs+ reduced the amplitude and/or duration of cyclic long-lasting hyperpolaryzations.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1993

Intracellular analysis of relations between the slow (< 1 Hz) neocortical oscillation and other sleep rhythms of the electroencephalogram.

The newly described slow cortical rhythm (approximately 0.3 Hz), whose depolarizing-hyperpolarizing components are analyzed in the preceding article, is now investigated from the standpoint of its relations with delta (1-4 Hz) and spindle (7-14 Hz) rhythmicity. Regular-spiking and intrinsically bursting cortical neurons were mostly recorded from association suprasylvian areas 5 and 7; fewer neurons were also recorded from pericruciate motor and posterolateral visual areas. Although most cells were investigated under various anesthetics, a similar slow cortical rhythm was found in animals with brainstem transection at the low- or high-collicular levels. These cerveau isolé (isolated forebrain) preparations display the major sleep rhythms of the EEG in the absence of general anesthetics. In 38% of recorded cortical neurons (n = 105), the slow rhythm was combined with delta oscillation. Both cellular rhythms were phase locked to the slow and delta oscillations in the surface- and depth-recorded EEG. In a group of this cell sample (n = 47), delta activity occurred as stereotyped, clock-like action potentials during the interdepolarization lulls of the slow rhythm. In another neuronal subsample (n = 58), delta events were grouped in sequences superimposed upon the depolarizing envelope of the slow rhythm, with such sequences recurring rhythmically at approximately 0.3-0.4 Hz. The associations between the two cellular and EEG rhythms (1-4 Hz and 0.3-0.4 Hz) were quantified by means of autocorrelograms, cross-correlograms, and spike-triggered averages. In 26% of recorded neurons (n = 72), the slow rhythm was combined with spindle oscillations. Regular-spiking cortical neurons fully reflected the whole frequency range of thalamically generated spindles (7-14 Hz). However, during similar patterns of EEG spindling, intrinsically bursting cells fired grouped action potentials (with intraburst frequencies of 100-200 Hz) at only 2-4 Hz. The dependence of the slow cortical oscillation upon the thalamus was studied by lesions and stimulation. The slow rhythm survived extensive ipsilateral thalamic destruction by means of electrolytic lesions or kainate-induced loss of perikarya in thalamic nuclei that were input sources to the recorded cortical neurons. To further prevent the possibility of a thalamic role in the genesis of the slow rhythm, through the contralateral thalamocortical systems and callosal projections, we also transected the corpus callosum in thalamically lesioned animals, and still recorded the slow rhythm in cortical neurons. These data indicate that the thalamus is not essentially implicated in the genesis of the slow rhythm.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1993

The slow (< 1 Hz) oscillation in reticular thalamic and thalamocortical neurons: scenario of sleep rhythm generation in interacting thalamic and neocortical networks.

As most afferent axons to the thalamus originate in the cerebral cortex, we assumed that the slow (< 1 Hz) cortical oscillation described in the two companion articles is reflected in reticular (RE) thalamic and thalamocortical cells. We hypothesized that the cortically generated slow rhythm would appear in the thalamus in conjunction with delta and spindle oscillations arising from intrinsic and network properties of thalamic neurons. Intracellular recordings have been obtained in anesthetized cats from RE (n = 51) and cortically projecting (n = 240) thalamic neurons. RE cells were physiologically identified by cortically evoked high-frequency spike bursts and depolarizing spindle oscillations. Thalamocortical cells were recognized by backfiring from appropriate neocortical areas, spindle-related cyclic IPSPs, and hyperpolarization-activated delta oscillation consisting of rhythmic low-threshold spikes (LTSs) alternating with afterhyperpolarizing potentials (AHPs). The slow rhythm (0.3-0.5 Hz) was recorded in 65% of RE neurons. In approximately 90% of oscillating cells, the rhythm consisted of prolonged depolarizations giving rise to trains of single action potentials. DC hyperpolarization increased the synaptic noise and, in a few cells, suppressed the long-lasting depolarizing phase of the slow rhythm, without blocking the fast EPSPs. In approximately 10% of oscillating neurons, the hyperpolarizing phase of the oscillation was much more pronounced, thus suggesting that the slow rhythm was produced by inhibitory sculpturing of the background firing. The slow oscillation was associated with faster rhythms (4-8 Hz) in the same RE neuron. The slow rhythm of RE neurons was closely related to EEG wave complexes recurring with the same frequency, and its strong dependency upon a synchronized state of cortical EEG was observed during shifts in EEG patterns at different levels of anesthesia. In 44% of thalamocortical cells the slow rhythm of depolarizing sequences was apparent and it could coexist with delta or spindle oscillations in the same neuron. The occurrence of the slowly recurring depolarizing envelopes was delayed by the hyperpolarizing spindle sequences or by the LTS-AHP sequences of delta oscillation. The hyperpolarization-activated delta potentials that tended to dampen after a few cycles were grouped in sequences recurring with the slow rhythm. We finally propose a unified scenario of the genesis of the three major sleep rhythms: slow, delta, and spindle oscillations.

Action Potentials↗
PubMed1992

Various types of inhibitory postsynaptic potentials in anterior thalamic cells are differentially altered by stimulation of laterodorsal tegmental cholinergic nucleus.

The effects of stimulating the laterodorsal tegmental cholinergic nucleus upon inhibitory postsynaptic potentials recorded in relay cells of the anterior thalamic complex were studied in urethane-anesthetized cats. The inhibitory postsynaptic potentials induced in anterior thalamic relay cells by stimulating mammillary nuclei or retrosplenial cortex are generated by local-circuit inhibitory neurons since this nuclear complex is devoid of afferents from the other intrathalamic source of inhibition, the reticular thalamic nucleus. In a parallel study from this laboratory, it has been shown that cortical stimulation elicits a biphasic inhibitory postsynaptic potential consisting of two (A and B) components attributed to axonal firing of local interneurons, whereas mammillary stimulation elicits, in addition to the A-B sequence, an earlier component (a) presumably generated by presynaptic dendrites in thalamic glomeruli. In the present study, short pulse-trains applied to the laterodorsal tegmental nucleus diminished the amplitudes of A and B inhibitory components or completely suppressed them. The B component was more sensitive to the depressive effect. By contrast with the changes of the A and B components, the mammillary-evoked a inhibitory component was not reduced and, in many instances, was enhanced following laterodorsal tegmental stimulation. The effects of laterodorsal tegmental stimulation survived monoamine depletion by reserpine. We suggest that mesopontine cholinergic depressive actions on A and B inhibitory postsynaptic potentials may be due to an increased conductance in thalamocortical cells during the short-lasting nicotinic action combined with a somatic hyperpolarization of local-circuit cells, whereas the enhancement of the earliest (a) inhibitory postsynaptic potential reflects a concomitant potentiating action at the level of intraglomerular presynaptic dendrites.

Animals↗
PubMed1992

Intrinsic and synaptically generated delta (1-4 Hz) rhythms in dorsal lateral geniculate neurons and their modulation by light-induced fast (30-70 Hz) events.

Thalamocortical neurons of cat dorsal lateral geniculate nucleus were recorded under urethane anesthesia. Neurons were identified by antidromic invasion from the internal capsule and by orthodromic stimulation from the optic chiasm or light stimuli. An intrinsic oscillation within the frequency of sleep delta waves (1-4 Hz) was induced by hyperpolarizing current pulses triggering a rhythmic sequence of low-threshold spikes alternating with after hyperpolarizing potentials. The increased propensity to oscillation after blockage of inputs arising in the retina indicates that afferent synaptic drives interfere with the intrinsic oscillation of lateral geniculate cells. The relatively rare occurrence of this type of oscillation in impaled neurons, as compared with extracellular recordings in the same nucleus or to intracellular recordings in other dorsal thalamic nuclei, suggests that the interplay between the two intrinsic currents generating delta oscillation is particularly critical in lateral geniculate cells. Another type of delta oscillation was characterized by excitatory postsynaptic potentials which gave rise to action potentials or to low-threshold spikes at more depolarized or hyperpolarized levels, respectively. It is suggested that this rhythm reflects synaptic coupling by intranuclear recurrent axonal collaterals. Light stimulation induced fast (30-70 Hz) excitatory events that were blocked after lidocaine injections into the eye. In all tested cells, changes in the ambient luminosity of the experimental room blocked the intrinsic as well as the synaptic oscillation within the delta frequency. In some cells, this suppressing effect was associated with depolarization and increased firing rate. These results demonstrate different types of sleep delta oscillations in visual thalamic neurons and show that they are modulated not only by brainstem regulatory systems, but also by specific drives along the visual channel.

Animals↗
PubMed1992

Delta frequency (1-4 Hz) oscillations of perigeniculate thalamic neurons and their modulation by light.

Neurons in the perigeniculate sector of the reticular thalamic nuclear complex were recorded extra- and intracellularly under deep urethane anesthesia. They were identified by burst responses to optic chiasm stimulation and depolarizing spindle oscillations in response to internal capsule stimulation. Perigeniculate neurons displayed oscillations within the frequency range of electroencephalogram delta waves (1-4 Hz). One-third of extracellularly recorded neurons discharged rhythmic (2.5-4 Hz), high-frequency (150-200 Hz) spike bursts. This was similar to an intrinsic oscillation that was recently observed in dorsal lateral geniculate cells studied in vitro and in vivo. Other oscillating neurons displayed trains of single spikes (20-50 Hz) crowning rhythmic (2.5-4 Hz) depolarizing envelopes that were best expressed at the "resting" membrane potential (-60 to -65 mV). It is suggested that this oscillation reflects synaptic drives from dorsal lateral geniculate neurons. Changes in ambient room luminosity disrupted both types of delta rhythms. These data demonstrate for the first time that delta oscillations are present in the visual sector of the reticular thalamic nucleus. The results suggest that the two types of delta rhythmicity result from intrinsic and network properties of visual thalamic neurons and that perigeniculate cells may synchronize, through backward connections, the activity of dorsal lateral geniculate cells during deep stages of resting sleep.

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PubMed1992

Intracellular evidence for incompatibility between spindle and delta oscillations in thalamocortical neurons of cat.

Recent studies have revealed that the thalamus does not only generate spindle oscillations (7-14 Hz), but that it also participates in the genesis of a slower (less than 4 Hz) rhythm within the frequency range of delta waves on the electroencephalogram. In thalamic cells, delta is an intrinsic oscillation consisting of low-threshold spikes alternating with afterhyperpolarizing potentials. It is known from electroencephalographic recordings in humans and animals that slow or delta waves prevail during late sleep stages, whereas spindle oscillations are characteristic for the early stages of sleep. We studied the dependence of spindles and delta oscillations on membrane potential, as well as the effects of spindles on delta oscillations, in thalamocortical neurons of cats under urethane anesthesia and in cerveau isolé preparations (low collicular transections). Spindles appeared at membrane potentials between -55 and -65 mV, whereas delta oscillations occurred by bringing the membrane potential between -68 and -90 mV. Spindles either evoked by cortical stimulation or occurring spontaneously in cerveau isolé preparations prevented delta oscillations. This effect was probably due to the increase in membrane conductance associated with spindles. Barbiturates also blocked delta activity in thalamocortical neurons, probably through the same mechanism. A certain degree of incompatibility between spindles and delta rhythms in thalamocortical cells may explain the prevalence of these two types of oscillations during different stages of sleep with synchronization of the electroencephalogram.

Animals↗
PubMed1992

Voltage-dependent fast (20-40 Hz) oscillations in long-axoned neocortical neurons.

Fast (20-80 Hz) oscillations of cortical activity, occurring during an increased level of focused alertness or elicited by optimal sensory stimuli, have been described by recording field potentials and neuronal firing in various cortical areas. Despite the increasing interest in this topic, little is known about the cellular mechanisms of the fast (generally termed 40-Hz) rhythm. An in vitro study demonstrated that, in sparsely spiny interneurons of frontal cortex, the 40-Hz rhythm is generated by a voltage-dependent persistent Na+ current, with the involvement of a delayed rectifier. Here we report depolarization-dependent 40-Hz oscillations in cat's motor and association neocortical neurons with identified projections to contralateral homotopic cortical area and thalamus. Our data indicate that this fast rhythm may be synchronized through intracortical and corticothalamic linkages.

Action Potentials↗
PubMed1992

Electrophysiology of a slow (0.5-4 Hz) intrinsic oscillation of cat thalamocortical neurones in vivo.

1. Electrophysiologically identified thalamocortical neurones have been intra- and extracellularly recorded in acutely prepared cats, under different anaesthetic conditions. 2. A slow (0.5-4 Hz) membrane potential oscillation was observed in thalamocortical cells recorded in motor, sensory, associational and intralaminar thalamic nuclei. The oscillation consisted of rhythmic low-threshold spikes alternating with after-hyperpolarizations. 3. About 80% of the neurones with intact cortical connections were set into the slow oscillatory mode by bringing their membrane potential to between -68 and -90 mV. The oscillation did not depend upon the occurrence of fast action potentials and did not outlast the imposed hyperpolarization. 4. Anatomical or functional disconnection from related cortical areas resulted in a membrane potential hyperpolarization of about 9 mV and in the occurrence of spontaneous slow oscillations in virtually all recorded neurones. The intrinsic nature of the phenomenon was supported by the lack of rhythmic postsynaptic potentials as the cells were prevented from oscillating by outward current injection. 5. In contrast with other thalamic nuclei, the slow oscillation has not been observed in anterior thalamic neurones despite their having similar basic electrophysiological properties. 6. Barbiturate administration suppressed the slow oscillatory mode, an effect accompanied by a decrease in the membrane input resistance. 7. Multiunit recordings of spontaneously oscillating cells showed epochs characterized by phase-related firing. This synchronous discharge was paralleled by a clear-cut build-up of field potentials in the frequency range of electroencephalogram slow or delta waves. 8. These results demonstrate that the majority of thalamocortical neurones are endowed with electrophysiological properties allowing them to oscillate at 0.5-4 Hz, if they have a membrane potential more negative than -65 mV and a high input resistance. Such a condition is physiologically achieved in the deepest stages of electroencephalogram-synchronized sleep, as a result of brain stem-thalamic as well as cortico-thalamic deafferentation. We postulate a thalamic contribution in the genesis of electroencephalogram delta waves during slow wave sleep, once independently oscillating thalamocortical cells become in phase.

Action Potentials↗
PubMed1992

Bursting and tonic discharges in two classes of reticular thalamic neurons.

1. Two types of cat reticular (RE) thalamic cells were disclosed by means of intracellular recordings under urethan anesthesia. The RE neurons were identified by their typical depolarizing spindle oscillations in response to synchronous stimulation of the internal capsule. 2. In type I neurons (n = 41), depolarizing current pulses induced tonic firing at the resting or slightly depolarized membrane potential (Vm) and triggered high-frequency spike bursts at a Vm more negative than -75 mV. As well, these cells discharged rebound bursts at the break of a hyperpolarizing current pulse. Internal capsule stimulation elicited spindle sequences made off by depolarizing waves giving rise to spike bursts. 3. Type II cells (n = 9) did not discharge spike bursts to large depolarizing current pulses even when the Vm reached -100 mV, nor did they fire rebound bursts after long-lasting hyperpolarizing current pulses or spike bursts riding on the rhythmic depolarizing components of spindle sequences. 4. Compared with type I cells, type II cells showed less frequency accommodation during tonic firing. The latter neuronal class discharged at high frequencies (40 Hz) with slight DC depolarization, approximately 8-10 Hz at the resting Vm, and no underlying synaptic or subthreshold oscillatory events could be detected when the firing was blocked by DC hyperpolarization. 5. The presence of two cell classes in the RE nucleus challenges the common view that this nucleus consists of a single neuronal class. We suggest that a different set of conductances is present in type II RE neurons, thus preventing the low-threshold Ca2+ current from dominating the behavior of these cells.

Animals↗
PubMed1992

Basic mechanisms of sleep generation.

Most brainstem, thalamic, and cortical cellular types undergo similar processes during rapid eye movement (REM) sleep and wakefulness, and both these brain-activated behavioral states are opposed to the resting EEG-synchronized sleep. Experimental evidence shows that during drowsiness, disfacilitation in thalamic and cortical neurons (by partial removal of influences from mesopontine, posterior hypothalamic, and basal forebrain activating systems) may coexist with active hypnogenic mechanisms. The idea of an active induction of sleep, however, still lacks firm support at the cellular level. The generation of REM sleep signs is probably caused, at least partially, by the disinhibition of mesopontine cholinergic cells, the executive elements of tonic and phasic events during dreaming sleep, following cessation of firing of inhibitory serotonergic dorsal raphe neurons.

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