Activity-dependent layer-specific changes in the extracellular chloride concentration and chloride driving force in the rat hippocampus.

The transmembrane distribution of chloride anions (Cl⁻) determines the direction of the Cl⁻ flux through GABA(A) receptors; this establishes whether GABA(A) receptor-mediated responses are hyperpolarizing or depolarizing in neurons. Thus an activity-dependent reduction in the efficacy of inhibitory responses can be the result of an activity-induced reduction of the Cl⁻ driving force. Using Cl(-)-sensitive electrodes, we measured the extracellular Cl⁻ concentration ([Cl⁻](o)) in each layer of the hippocampus under control conditions and after stimulation. In the control condition, [Cl⁻](o) was lower within the CA1 region (112.9 ± 1.3 mM; mean ± SD) than the CA3/dentate gyrus areas (117.7 ± 1.2 mM). Stimulation of CA3 pyramidal cells led to an increase in the [Cl⁻](o). The maximum values were observed in the stratum lacunosum-moleculare (253.4 ± 51.1 mM) and in the hilus (261 ± 43.7 mM), whereas in the granular cell layer, it reached only 159.5 ± 41 mM. The stimulation-induced [Cl⁻](o) increase was followed by a period of decreasing [Cl⁻](o) that fell below the control values. The maximum undershoot (21.6 ± 0.7 mM) was observed in the s. radiatum. Systemic application of the gap junction blocker carbenoxolone significantly decreased the stimulation-induced Cl⁻ extrusion in the dentate gyrus but only slightly modified it in the CA1 area. Carbenoxolone also drastically reduced the Cl⁻ clearance. The time constant of the Cl⁻ clearance was similar between layers (83.4 ± 15.9 ms) but increased after carbenoxolone application (207.1 ± 44.4 ms). Stimulation-induced changes in the [Cl⁻](o) significantly decreased the Cl⁻ driving force and resulted in large fluctuations between layers (Δ = 9.4 mV). The lowest value was observed in the stratum radiatum of the CA1 and the hilar region (7.7 mV), whereas the highest value was calculated for the granule cell layer (16.3 mV). We suggest that a decrease of the extracellular space is mainly responsible for the rapid [Cl⁻](o) increase while the gap junction coupled astrocytic network plays a key role in the activity-dependent redistribution and clearance of Cl⁻ across layers of the hippocampus.

Synchronized sleep oscillations and their paroxysmal developments.

The state of resting sleep is associated with a series of oscillations generated in cortical and thalamic networks. A newly discovered rhythm groups the spindle and delta sleep oscillations within slowly recurring (< 1 Hz) sequences. Multi-site, extra- and intracellular recordings provide evidence for synchronization of various classes of cell in the neocortex and thalamus during sleep oscillations that might reach paroxysmal levels similar to epileptic states. Sleep oscillations and the underlying synchronizing processes are disrupted during transition to brain arousal.

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.

Cellular substrates and laminar profile of sleep K-complex.

We describe the cellular mechanisms that underlie the generation of the K-complex, a major grapho-element of sleep electroencephalogram in humans. First we demonstrate the similarity between K-complexes recorded during natural sleep and under ketamine-xylazine anaesthesia in cats. Thereafter, we show by means of multi-site cellular and field potential recordings that K-complexes are rhythmic at frequencies of less than 1 Hz (mainly 0.5-0.9 Hz) and that they are synchronously distributed over the whole cortical surface as well as transferred to the thalamus. The surface K-complex reverses its polarity at a cortical depth of about 0.3 mm. At the cortical depth, the K-complex is made of a sharp and high-amplitude negative deflection that reflects cellular depolarization, often preceded by a smaller-amplitude, positive slow-wave reflecting cellular hyperpolarization. The sharp component of the K-complex may lead to a spindle sequence and/or to fast (mainly 20-50 Hz) oscillations. K-complexes appear spontaneously or triggered by cortical or thalamic stimulation, and they arise within cortical networks. We suggest that K-complexes, either in isolation or followed by a brief sequence of spindle waves, are the expression of the spontaneously occurring, cortically generated slow oscillation.

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.

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.

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.

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.

Changes in neuronal conductance during different components of cortically generated spike-wave seizures.

Neuronal conductance was studied in anesthetized cats during cortically generated spike-wave seizures arising from slow sleep oscillation. Single and dual intracellular recordings from neocortical neurons were used. The changes were similar whether the seizures occurred spontaneously, or were evoked by electrical stimulation or induced by bicuculline. In all seizures, the conductance increased from the very onset of the seizure and returned to control values only at the end of the postictal depression. Simultaneous intracellular recordings from two neurons showed that the neuron leading the other neuron displayed the largest increase in membrane conductance. The changes in neuronal conductance during the two phases of the slow sleep oscillation, i.e. highest during depolarizations and lowest during hyperpolarizations, were similar to those occurring during the "spike" and "wave" components of seizures. (1) Maximal conductance was found during the paroxysmal depolarizing shift corresponding to the electroencephalogram "spike" (median: 252 nS; range: 90 to more than 400 nS). It was highest at the onset of the depolarized plateau and decreased thereafter. (2) During the hyperpolarization corresponding to the electroencephalogram "wave", the conductance was significantly lower (median: 71 nS; range: 41 to 140 nS). (3) The conductance was elevated during the fast runs (median: 230 nS; range: 92 to 350 nS) which occurred in two-thirds of the seizures. (4) The conductance values during postictal depression were situated between those measured during the seizure hyperpolarizations and during sleep hyperpolarizations. The conductance decreased exponentially back to the values of the slow sleep oscillation over the total duration of the postictal depression. The data suggest that the major mechanism underlying the "wave"-related hyperpolarizing component of spike-wave seizures relies mainly not on active inhibition, but on a mixture of disfacilitation and potassium currents.

The brain decade in debate: VII. Neurobiology of sleep and dreams.

This article is a transcription of an electronic symposium held on February 5, 2001 by the Brazilian Society of Neuroscience and Behavior (SBNeC) during which eight specialists involved in clinical and experimental research on sleep and dreaming exposed their personal experience and theoretical points of view concerning these highly polemic subjects. Unlike most other bodily functions, sleep and dreaming cannot, so far, be defined in terms of definitive functions that play an ascribable role in maintaining the organism as a whole. Such difficulties appear quite clearly all along the discussions. In this symposium, concepts on sleep function range from a protective behavior to an essential function for maturation of the nervous system. Kleitman's hypothesis [Journal of Nervous and Mental Disease (1974), 159: 293-294] was discussed, according to which the basal state is not the wakeful state but sleep, from which we awake to eat, to protect ourselves, to procreate, etc. Dreams, on the other hand, were widely discussed, being considered either as an important step in consolidation of learning or simply the conscious identification of functional patterns derived from the configuration of released or revoked memorized information.

Integration of low-frequency sleep oscillations in corticothalamic networks.

The corticothalamic system acts as a complex network in promoting the various oscillatory patterns (slow oscillation, spindles, delta) that characterize the state of quiet sleep. Local synchronizing mechanisms of any of the above-mentioned oscillations occur at the site of their genesis, thalamic or cortical. These mechanisms are assisted by the wide-range, synchronized occurrence of the cortical slow oscillation, which finally produces the coalesced picture of slow-wave sleep EEG. Multisite, simultaneous intracellular and field potential recordings in cat, as well as EEG recordings in human were performed in order to assess the state of synchrony and the propagation of various sleep rhythms in the corticothalamic network.

[The mechanisms behind the generation of the slow oscillations found in EEG recordings during sleep]. / Mecanismos de generación de las oscilaciones lentas del electroencefalograma durante el sueño.

INTRODUCTION: Electroencephalogram (EEG) recordings reflect different oscillatory activities during slow wave sleep (stages 2 and 3-4 of the sleep-waking cycle), namely d oscillations (< 4 Hz), sleep spindles and K complexes. These activities are essentially generated by the activity of the thalamo-cortical relay neurons, the neurons of the thalamic reticular nucleus and by the neurons in the cerebral cortex. DEVELOPMENT: The combination of the intrinsic electrophysiological properties of the thalamic and cortical neurons, together with their synaptic connections, are responsible for the generation of these oscillations. Extra or intracellular recordings of these neurons during spontaneous or anaesthetic-induced sleep show how these neurons change their electrical activity during slow sleep due to the hyperpolarization of their membrane potential. Thus, the thalamic neurons lower their response to sensory stimuli and filter this information towards the cerebral cortex. Glial cells also contribute to the generation of the d waves seen in the EEG and oscillate synchronously with the cortical neurons. In addition, the oscillations of this neuronal and glial network is linked to important changes in the concentration of certain ions in the extracellular space; for instance, the K+ and Ca2+ concentration oscillates synchronously with the neuronal and the glial activity. CONCLUSIONS: The oscillations in the EEG, which are slower than those observed in the waking state or in paradoxical sleep, play a fundamental role in processing the information handled by the central nervous system and filter the irrelevant information towards the cerebral cortex.

Dynamic coupling among neocortical neurons during evoked and spontaneous spike-wave seizure activity.

1. We investigated the development from patterns of electroencephalogram (EEG) synchronization to paroxysms consisting of spike-wave (SW) complexes at 2-4 Hz or to seizures at higher frequencies (7-15 Hz). We used multisite, simultaneous EEG, extracellular, and intracellular recordings from various neocortical areas and thalamic nuclei of anesthetized cats. 2. The seizures were observed in 25% of experimental animals, all maintained under ketamine and xylazine anesthesia, and were either induced by thalamocortical volleys and photic stimulation or occurred spontaneously. Out of unit and field potential recordings within 370 cortical and 65 thalamic sites, paroxysmal events occurred in 70 cortical and 8 thalamic sites (approximately 18% and 12%, respectively), within which a total of 181 neurons (143 extracellular and 38 intracellular) were simultaneously recorded in various combinations of cell groups. 3. Stimulus-elicited and spontaneous SW seizures at 2-4 Hz lasted for 15-35 s and consisted of barrages of action potentials related to the spiky depth-negative (surface-positive) field potentials, followed by neuronal silence during the depth-positive wave component of SW complexes. The duration of inhibitory periods progressively increased during the seizure, at the expense of the phasic excitatory phases. 4. Intracellular recordings showed that, during such paroxysms, cortical neurons displayed a tonic depolarization (approximately 10-20 mV), sculptured by rhythmic hyperpolarizations. 5. In all cases, measures of synchrony demonstrated time lags between discharges of simultaneously recorded cortical neurons, from as short as 3-10 ms up to 50 ms or even longer intervals. Synchrony was assessed by cross-correlograms, by a method termed first-spike-analysis designed to detect dynamic temporal relations between neurons and relying on the detection of the first action potential in a spike train, and by a method termed sequential-field-correlation that analyzed the time course of field potentials simultaneously recorded from different cortical areas. 6. The degree of synchrony progressively increased from preseizure sleep patterns to the early stage of the SW seizure and, further, to its late stage. In some cases the time relation between neurons during the early stages of seizures was inversed during late stages. 7. These data show that, although the common definition of SW seizures, regarded as suddenly generalized and bilaterally synchronous activities, may be valid at the macroscopic EEG level, cortical neurons display time lags between their rhythmic spike trains, progressively increased synchrony, and changes in the temporal relations between their discharges during the paroxysms.(ABSTRACT TRUNCATED AT 400 WORDS)

Sleep oscillations developing into seizures in corticothalamic systems.

PURPOSE: The aim of this article is to discuss the neuronal substrates of sleep oscillations leading to seizures consisting of spike-wave (SW) complexes at 2-4 Hz, mimicking those seen in absence epilepsy, or SW and polyspike-wave (PSW) complexes at 1.5-2.5 Hz, often associated with fast runs at 10-15 Hz, as in the Lennox-Gastaut syndrome. METHODS: Extracellular recordings were done in permanently implanted animals during the natural waking-sleep cycle. Single and dual simultaneous recordings from cortical neurons, cortical and thalamic neurons, or cortical neurons and glial cells were performed in cats under ketamine-xylazine anesthesia. RESULTS: (a) The minimal substrate of SW seizures is the neocortex because such seizures may occur in thalamectomized animals, in which spindles are absent. In intact-brain animals, SW seizures are initiated in neocortex and spread to the thalamus after a few seconds. The majority of thalamocortical (TC) neurons are steadily hyperpolarized throughout the cortical SW seizures. (b) In the Lennox-Gastaut syndrome, the paroxysmal depolarizing shifts (PDSs) associated with the EEG "spike" of SW/PSW complexes contain an important inhibitory component, whereas the hyperpolarization during the EEG "wave" component is not due to gamma-aminobutryic acid (GABA)ergic inhibitory postsynaptic potentials (IPSPs) but is ascribed to a mixture of disfacilitation and K+ currents. As is also the case with seizures consisting of pure SW complexes, the majority of TC neurons are hyperpolarized during the cortical paroxysms and disinhibited after the cessation of cortical seizures. CONCLUSIONS: Seizures with SW complexes and of the Lennox-Gastaut type preferentially evolve from sleep oscillations. They are initiated in neocortex and spread to the thalamus after a few seconds. The majority of TC neurons are inhibited during these seizures.

Short- and long-range neuronal synchronization of the slow (< 1 Hz) cortical oscillation.

1. Multisite, extra- and intracellular recordings were carried out in cats under ketamine and xylazine anesthesia to assess the degree of synchrony and time relations among cellular activities in various neocortical fields during a slow (< 1 Hz) oscillation consisting of long-lasting depolarizing and hyperpolarizing phases. 2. Recordings were performed from visual areas 17, 18, 19, and 21, association suprasylvian areas 5 and 7, motor pericruciate areas 4 and 6, as well as some related thalamic territories, such as the lateral geniculate (LG), perigeniculate (PG), and rostral intralaminar nuclei. We used spike analyses (auto- and cross-correlograms) to reveal rhythmicities, time relations and coherence properties, analyses of field potentials recorded through the same microelectrodes as used for unit discharges (auto-and cross-correlation functions and their spectral equivalents), and spike-triggered averages. The results are based on 194 groups of neurons with a total of 591 neurons. Seventeen groups included intracellular recordings of cortical neurons with membrane potentials more negative than -60 mV and overshooting action potentials. 3. The most obvious and frequent signs of neuronal synchrony were found within and between association areas 5 and 7 and 18/19 and 21. Closely located cells or neuronal pools were also "closer" in time. The shortest mean time lag was found between cells within adjacent foci (1-2 mm) of areas 5 and 7 and was 12 +/- 11.2 (SE) ms, with more caudal neurons preceding the rostral ones in 70% of cases. In visual cortical fields, the time lag between areas 18/19 and 21 neurons was 27.6 +/- 36 ms, between areas 17 and 21 was 36.2 +/- 47.8 ms, and between areas 18/19 and 17 was 40 +/- 73 ms. In the majority of cases, neuronal firing in area 21 preceded that in areas 18/19. The longest time lags were found in distant recordings from visual and motor areas, with a mean of 124 +/- 86.8 ms, although in some cell groups the time intervals between neuronal firing in areas 18/19 or 21 and areas 4 or 6 were as short as approximately 20 ms. 4. Similar time relations were found in those instances in which the unit firing of the same cortical neuron was used as reference in spike triggered averages and was related to the field potential recorded from an adjacent area before impaling a neuron and, thereafter, to membrane potential fluctuations after impaling the cell. 5. The PG reticular thalamic neurons reflected the slow cortical oscillation in 75% of multisite recordings.(ABSTRACT TRUNCATED AT 400 WORDS)

Coalescence of sleep rhythms and their chronology in corticothalamic networks.

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.

Slow sleep oscillation, rhythmic K-complexes, and their paroxysmal developments.

This paper presents the relations between the slow (< 1 Hz) oscillation (characterizing the activity of corticothalamic networks during quiescent sleep in cats and humans), sleep K-complexes, and some paroxysmal developments of sleep patterns. At the cellular level, the slow oscillation is built up by rhythmic membrane depolarizations and hyperpolarizations of cortical neurons. The EEG expression of this activity is marked by periodic K-complexes which reflect neuronal excitation. The slow oscillation triggers, groups and synchronizes other sleep rhythms, such as thalamically generated spindles as well as thalamically and cortically generated delta oscillations. We discuss the distinctness of the slow (< 1 Hz) and delta (1-4 Hz) oscillations. We also show that the slow cortical oscillation underlies the onset of spike-wave seizures during sleep by transforming the periodic K-complexes into recurrent paroxysmal spike-wave complexes.

Disconnection of intracortical synaptic linkages disrupts synchronization of a slow oscillation.

The intracortical synaptic linkages underlying the synchronization of a recently described slow (< 1 Hz) oscillation (Steriade et al., 1993b,c) were investigated in anesthetized cats by means of multisite extra- and intracellular recordings, including dual impalements, from rostral and caudal sites in the association cortical suprasylvian and marginal gyri, before and after reversible lidocaine inactivation or transections in the middle suprasylvian gyrus. Stimulus-evoked responses revealed that the rostral and caudal suprasylvian foci are reciprocally connected, with a preference for posterior-to-anterior responses. Lidocaine infusion between the stimulating and recording sites disrupted the intracortical synaptic linkage, while leaving unaffected the responses at the sites close to the stimulating electrodes. The high coherence between slowly oscillating field potentials and intracellular activities recorded from anterior and posterior suprasylvian foci was lost after reversible inactivation or transections in the middle suprasylvian gyrus, whereas the synchrony between adjacent foci within the anterior or posterior areas was preserved. Two to four hours after inactivation or transection the synchrony between all channels was totally or partially recovered. We introduced the synchrony coefficient (SyCo) and calculated the SyCo for closely located and distant sites. Lidocaine infusion or transection did not affect the SyCo between leads placed on the same site, but significantly (60%) decreased the SyCo between channels separated by the functionally inactivated or transected sector. Our results demonstrate that pathways within or beneath the suprasylvian gyrus sustain the synchronization of the slow oscillation between cortical sites. As the loss of long-range coherence was not permanent, intergyral paths and/or corticothalamocortical loops may exert compensatory functions after the disconnection of intrasuprasylvian synaptic linkages.

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].

Extracellular calcium fluctuations and intracellular potentials in the cortex during the slow sleep oscillation.

During slow wave sleep the main activity of cortical neurons consists of synchronous and rhythmic alternations of the membrane potential between depolarized and hyperpolarized values. The latter are long-lasting (200-600 ms) periods of silence. The mechanisms responsible for this periodical interruption of cortical network activity are unknown. Here we report a decrease of approximately 20% in the extracellular calcium concentration ([Ca](out)) progressively taking place in the cortex between the onset and the offset of the depolarizing phase of the slow sleep oscillation. Since [Ca](out) exerts a high gain modulation of synaptic transmission, we estimated the associated transmitter release probability and found a corresponding 50% drop. Thus the periods of silence occurring in the cortical network during slow wave sleep are promoted by recurrent [Ca](out) depletions.