Biomedical subjects

F Amzica

Publications and source records attributed to F Amzica.

35 records · Page 2Linked to original sources

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

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

Synchronization of fast (30-40 Hz) spontaneous cortical rhythms during brain activation.

We investigated the synchronization of fast spontaneous oscillations (mainly 30-40 Hz) in anesthetized and behaving cats by means of simultaneous extra- and intracellular recordings from multiple neocortical areas. Fast Fourier transforms, auto- and cross-correlations, and spike- or wave-triggered averages were used to determine the frequency and temporal coherence of fast oscillations that outlasted the stimulation of ascending activating systems or that occurred naturally during behavioral states of waking and rapid eye movement (REM) sleep but also appeared during the depolarizing phases of slow sleep oscillations. In 90% of microelectrode tracks, the fast oscillations did not show field reversal at any depth of the cortex and were not observable in the underlying white matter. The negative field potentials of the fast oscillations were associated at all depths with neuronal firing. This field potential property of fast oscillations was in sharp contrast to the reversal of slow sleep oscillation or evoked potentials at depths of 0.25-0.5 mm. The coherence of fast spontaneous rhythms was spatially limited, being confined within a cortical column and among closely located neocortical sites, in contrast to the long-range synchronization of slow sleep rhythms. Depolarizing current pulses elicited spike-bursts (200-400 Hz) recurring at a frequency of 30-40 Hz. Our experiments demonstrate that the conventional notion of a totally desynchronized cortical activity upon arousal should be revised as fast rhythms are enhanced and synchronized within intracortical networks during brain activation. Spontaneously occurring, subthreshold membrane potential depolarizing oscillations may bias cortical and thalamic neurons to respond synchronously, at fast frequencies, to relevant stimuli in the wake state or to internally generated drives in REM sleep.

Animals↗

PubMed1995

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)

Animals↗

PubMed1995

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.

Action Potentials↗

PubMed1994

Cortical and thalamic cellular correlates of electroencephalographic burst-suppression.

This experimental study on anesthetized cats used intracellular recordings of cortical, thalamocortical and reticular thalamic neurons (n = 54), as well as multi-site extracellular recordings (n = 36), to investigate the cellular correlates of EEG burst-suppression patterns, defined as alternating wave bursts and periods of electrical silence. Burst-suppression was elicited by the administration of the same or other anesthetic agents upon the background of an already synchronized EEG activity. About 95% of cortical cells entered burst-suppression, in close time-relation with EEG activity, displaying sequences of phasic depolarizing events associated with bursts of EEG waves and an electrical silence of the neuronal membrane during flat EEG epochs. The membrane potential (Vm) hyperpolarized by approximately 10 mV prior to any EEG change and the slow rhythms reflecting deep stages of anesthesia progressively disorganized with transition to burst-suppression. During flat EEG epochs, the apparent input resistance (tested through short hyperpolarizing current pulses) decreased (range 12-60%) and neuronal responsiveness to orthodromic volleys (tested by thalamic and cortical evoked excitatory postsynaptic potentials) was dramatically reduced. It is proposed that the decreased input resistance is mainly due to an increase in K+ conductances. At variance with cortical neurons, only 60-70% of thalamic cells ceased firing before overt EEG burst-suppression and were completely silent during flat periods of EEG activity. The remaining 30-40% of thalamic cells discharged rhythmic (1-4 Hz) spike bursts during periods of EEG silence. This rhythm, within the frequency range of delta waves, is generated in thalamic cells by the interplay between two of their intrinsic currents at critical levels of Vm hyperpolarization. However, with the deepening of burst-suppression, when silent EEG periods became longer than 30 sec, thalamic cells also ceased firing. The assumption that full-blown burst-suppression is achieved through virtually complete disconnection in brain circuits implicated in the genesis of the EEG is corroborated by the revival of normal cellular and EEG activities after volleys setting into action thalamic and cortical networks.

Animals↗

PubMed1994

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.

Animals↗

PubMed1994

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)

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)

Animals↗

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)

Animals↗

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↗

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.

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↗

PubMedDate not supplied

[The mechanisms behind the generation of the slow oscillations found in EEG recordings during sleep].

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.

Cerebral Cortex↗