Search PubMed⌕ Search

Biomedical subjects

M Steriade

Publications and source records attributed to M Steriade.

At least 91 records · Page 5Linked to original sources

In vivo, in vitro, and computational analysis of dendritic calcium currents in thalamic reticular neurons.

Thalamic reticular (RE) neurons are involved in the genesis of synchronized thalamocortical oscillations, which depend in part on their complex bursting properties. We have investigated the intrinsic properties of RE cells using computational models based on morphological and electrophysiological data. Simulations of a reconstructed RE cells were compared directly with recordings from the same cell to obtain precise values for the passive parameters. In a first series of experiments, the low-threshold calcium current (I(Ts)) was studied via voltage clamp in acutely dissociated RE cells that lack most of their dendrites. Simulations based on a cell with truncated dendrites and Hodgkin-Huxley kinetics reproduced these recordings with a relatively low density of I(Ts). In a second series of experiments, voltage-clamp recordings obtained in intact RE cells in slices showed a higher amplitude and slower kinetics of I(Ts). These properties could be reproduced from the reconstructed cell model assuming higher densities of I(Ts) in distal dendrites. In a third series of experiments, current-clamp recordings were obtained on RE cells in vivo. The marked differences with in vitro recordings could be reconciled by simulating synaptic bombardment in the dendrites of RE cells, but only if they contained high distal densities of I(Ts). In addition, simpler models with as few as three compartments could reproduce the same behavior assuming dendritic I(Ts). These models and experiments show how intrinsic bursting properties of RE cells, as recorded in vivo and in vitro, may be explained by dendritic calcium currents.

Animals↗

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↗

Two channels in the cerebellothalamocortical system.

Two channels of the cerebellothalamocortical system were investigated in cats by using cerebellar-evoked synaptic responses and cortical-evoked antidromic invasion of single thalamic cells. One channel arises in interpositus and dentate cerebellar nuclei and mainly projects through ventroanterior-ventrolateral (VA-VL) thalamic nuclei to cortical motor areas 4 and 6; the other channel arises in cerebellar fastigial nuclei and projects through ventromedial (VM) thalamic nuclei to more widespread cortical areas. The antidromic response latencies of VM neurons to stimuli applied to cortical areas 4 and 6 were longer (medians 2.8 and 3.0 msec, respectively) than the antidromic response latencies of VA-VL neurons to stimulation of the same cortical areas (1.8 and 2.3 msec). This was a statistically significant difference, and it matched the longer latencies of fastigial-evoked synaptic responses of VM cells (2.9 msec) compared to the response latencies of VA-VL cells elicited by stimulation of interpositus or dentate nuclei (1.7 and 2.4 msec). These differences among thalamic nuclei relaying cerebellocortical impulses were corroborated by dissimilar effects exerted on the electroencephalogram (EEG) during high-frequency (300 Hz) pulse trains applied to different deep cerebellar nuclei. The distribution of activated EEG patterns over the cortex depended on the stimulated site. Fastigial stimulation elicited the blockage of slow EEG rhythms and the appearance of fast oscillations (20-40 Hz) over widespread cortical areas in the proreus, pericruciate, and suprasylvian gyri. At variance, the activating influence of interpositus or dentate nuclei was restricted to the motor cortex. It is proposed that, besides their role in controlling the postural axial and proximal musculature, fastigial nuclei are part of diffusely activating systems.

Animals↗

Sleep electroencephalography and the clinical response to amitriptyline in patients with fibromyalgia.

OBJECTIVE: To determine the prevalence and clinical correlations of an anomaly consisting of electroencephalographic (EEG) waves within the alpha frequency band during non-rapid eye movement (NREM) sleep in patients with fibromyalgia, and to evaluate the alpha NREM sleep anomaly as a predictor of response to amitriptyline. METHODS: Twenty-two patients with fibromyalgia were studied in a 2-month, double-blind, crossover trial of amitriptyline (25 mg/day) versus placebo. Nocturnal EEGs were conducted on 2 consecutive nights at baseline and at the end of each 2-month treatment period. RESULTS: Six patients (27%) had a clinical response to amitriptyline, while none responded to placebo (P = 0.02). Treatment with amitriptyline or placebo did not result in any changes in the alpha ratings during NREM sleep. Only 8 patients (36%) exhibited the alpha NREM sleep anomaly at baseline. Those patients reported more sleep difficulty, but otherwise were clinically indistinguishable from those without this EEG sleep anomaly. Lower baseline alpha NREM sleep ratings were seen in responders to amitriptyline than in nonresponders, but these differences did not reach statistical significance. CONCLUSION: The alpha NREM sleep anomaly is present in only a small proportion of patients with fibromyalgia. It does not correlate with disease severity nor is it affected by treatment with amitriptyline. A larger sample size will be needed to adequately assess the value of this sleep anomaly in predicting the response to amitriptyline.

Adult↗

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↗

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↗

Cellular basis of EEG slow rhythms: a study of dynamic corticothalamic relationships.

A slow oscillation (< 1 Hz) has recently been described in intracellular recordings from the neocortex and thalamus (Steriade et al., 1993c-e). The aim of the present study was to determine the phase relations between cortical and thalamic neuronal activities during the slow EEG oscillation. Intracellular recordings were performed in anesthetized cats from neurons in motor and somatosensory cortical areas, the rostrolateral sector of the reticular (RE) thalamic nucleus, and thalamocortical (TC) cells from ventrolateral (VL) nucleus. The EEG was used as time reference for alignment of activities in different, simultaneously recorded neurons, including dual impalements of cortical cells as well as cortical and TC cells. The spontaneous EEG oscillation was characterized by slowly recurring (0.3-0.9 Hz) sequences of surface-positive (depth-negative) sharp deflections, often followed by oscillatory activity within the frequency range of sleep spindles (7-14 Hz) or at faster frequencies. Cortical and RE cells were similarly hyperpolarized during the depth-positive EEG waves and were depolarized during the depth-negative EEG deflections. In many instances, the cell depolarization was associated with oscillations at the spindle frequency or with tonic firing at rates related to the level of depolarization. TC neurons were hyperpolarized during the depth-positive EEG waves and displayed a series of IPSPs, at the spindle frequencies, during the depth-negative EEG waves. Depending on the membrane potential (Vm), TC cells could fire spike bursts at the onset of the EEG depth-negativity, or their firing could be delayed by subsequent IPSPs. The sequence of spontaneous EEG and cellular events described above also characterized the responses to cortical and thalamic stimulation. Simultaneous intracellular recordings of pairs of cortical cells or cortical and TC cells showed that spontaneous transitions from less synchronized to more synchronized EEG states were marked by a simultaneous hyperpolarization, coincident with an overt depth-positive EEG wave. We conclude that during low-frequency oscillatory states, characteristic of slow-wave sleep, neocortical and thalamic neurons display phase relations that are restricted to narrow time windows, and that synchronization results from a generalized inhibitory phenomenon. Moreover, EEG synchronization is reflected as active inhibition in TC neurons. That this pattern is also present in states of hypersynchronization, such as seizure activity, is shown in the following paper (Steriade and Contreras, 1994).

Animals↗

Relations between cortical and thalamic cellular events during transition from sleep patterns to paroxysmal activity.

We investigated in anesthetized cats the progressive development from EEG-synchronized sleep patterns to low-frequency (< 15 Hz) paroxysmal activities, most of them consisting of epileptic-like seizures with spike-wave (SW) complexes at 2-4 Hz. We used multisite extra- and intracellular recordings of neocortical, reticular thalamic (RE), and thalamocortical (TC) neurons, including dual impalements of cortical and TC cells. A subsample (40%) of TC cells discharged spike bursts at 2-4 Hz, in close time relation with the spiky, depth-negative field components of SW seizures in related neocortical areas. Full synchronization among TC cells that were resonant with the cortical seizure activity was progressively reached toward the end of the SW paroxysm. The remaining TC cells (60%) were inhibited during the cortical SW seizures. We show that the duration and amplitude of hyperpolarization in TC cells paralleled the extent of cortical EEG paroxysm. Dual intracellular recordings of cortical and TC neurons demonstrate that during the cortical SW seizure, consisting of a tonic depolarization with superimposed paroxysmal spike bursts, the simultaneously recorded TC neurons displayed a tonic hyperpolarization associated with repetitive IPSPs, closely time related with cortical cell bursts. The inhibition of TC cells was presumably mediated by GABAergic RE thalamic neurons. Indeed, simultaneously recorded RE and TC neurons during the cortical SW paroxysm showed that cortical and RE cell excitation was accompanied by corresponding IPSPs in TC cells. We emphasize the progressive development from sleep patterns to some forms of epileptic-like activities. We propose that the inhibitory processes found in a significant number of TC cells during cortical SW seizures may contribute to the loss of consciousness, due to obliteration of synaptic transmission through the thalamus.

Animals↗

Brain activation, then (1949) and now: coherent fast rhythms in corticothalamic networks.

The hypothesis of forebrain activation elicited by brainstem reticular core stimulation, formulated almost a half century ago, is now fully substantiated at the intracellular level of thalamic and neocortical neurons. Data show that stimulation of mesopontine cholinergic nuclei induces a prolonged muscarinic depolarization of thalamocortical neurons, associated with an increase in their apparent input resistance (that explains the enhanced probability of thalamic responses to incoming volleys upon arousal) and accompanied by a long-lasting activation of cortical rhythms. Activation also includes the preservation or even enhancement of short-lasting sculpturing inhibitory processes in thalamic and neocortical cells, a basic requirement for discrimination purposes. The notion of activation, that was erroneously termed as a "desynchronized" activity in thalamocortical networks, is now demonstrated to include spontaneously occurring, synchronous fast (20-40 Hz) rhythms. While the spatial coherence of sleep rhythms extends over wide territories, fast oscillations during brain arousal are synchronous within a cortical column and among closely spaced cortical areas, thalamic nuclei, and corticothalamic systems. Fast oscillations do not exclusively characterize brain-active states of waking and REM sleep, as they are also present during the depolarizing phase of the slow sleep oscillation in both cortical and thalamic cells. The subthreshold fast depolarizing spontaneous oscillations may bias thalamic and cortical cells to respond synchronously, at fast frequencies, to external stimuli in the wake state and to internal drives (such as ponto-geniculo-occipital signals) during REM sleep.

Acetylcholine↗

Modeling the control of reticular thalamic oscillations by neuromodulators.

Compartmental models of thalamic reticular (RE) neurons were investigated based on current-clamp and voltage-clamp data. Spontaneous oscillations in the model arise from the interaction between inhibitory synaptic currents and the rebound burst of RE cells. These oscillations critically depend on the level of the resting membrane potential. A network of RE neurons can be switched between silent and sustained oscillatory behavior by modulating a leak potassium current through neuromodulatory synapses. These results suggest that neuromodulators, such as noradrenaline, serotonin and glutamate, can exert a decisive control over the oscillatory activity of systems of RE cells. The model may explain why the isolated RE nucleus oscillates spontaneously in vivo but not in vitro.

Electrophysiology↗

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↗

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↗

A model of spindle rhythmicity in the isolated thalamic reticular nucleus.

1. The oscillatory properties of the isolated reticular (RE) thalamus were modeled with the use of compartmental models of RE cells. Hodgkin-Huxley type kinetic models of ionic channels were derived from voltage- and current-clamp data from RE cells. Interactions between interconnected RE cells were simulated with the use of a kinetic model of gamma-aminobutyric acid (GABA) inhibitory synapses. 2. The intrinsic bursting properties of RE cells in the model were due to the presence of a low-threshold Ca2+ current and two Ca(2+)-activated currents. The properties of these model RE cells were compared with RE neurons recorded intracellularly in vivo in cats. 3. Model RE cells densely interconnected with GABAA synapses produced synchronous oscillations at a frequency close to that of spindles (7-14 Hz). Networks of RE neurons organized in a two-dimensional array with only proximal connectivity also exhibited synchronized oscillations in the spindle range. In addition, the proximally connected network showed periods of high and low synchronicity, giving rise to waxing and waning oscillations in the population of RE cells. 4. The spatiotemporal behavior of the network was investigated during waxing and waning oscillations. The waxing and waning emerged as an alternation between periods of desynchronized and synchronized activity, corresponding to periods of irregular and coherent spatial activity. During synchronized periods, the network displayed propagating coherent waves of synchronous activity that had a tendency to form spirals. 5. Networks of model RE neurons fully connected through GABAB synapses exhibited perfectly synchronous oscillations at lower frequencies (0.5-1 Hz), but two-dimensional networks with proximal GABAB connectivity failed to synchronize. 6. These simulations demonstrate that networks of model neurons that include the main intrinsic currents found in RE cells can generate waxing and waning oscillatory activity similar to the spindle rhythmicity observed in the isolated RE nucleus in vivo. The model reveals the interplay between the intrinsic rhythmic properties of RE cells and the fast synaptic interactions in organizing synchronized rhythmicity.

Afferent Pathways↗

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↗

Sleep oscillations and their blockage by activating systems.

There are three major oscillations in thalamocortical systems during the state of sleep with synchronization of the electroencephalogram: 1. Spindles (7 Hz to 14 Hz) are generated in the thalamus at sleep onset and are blocked during arousal or rapid-eye-movement sleep by cholinergic systems that decouple the synchronizing network of the reticular thalamic nucleus. 2. Delta potentials (1 Hz to 4 Hz) appear during late stages of electroencephalogram-synchronized sleep. At the thalamic level they are produced by the interplay between two intrinsic currents of neurons with cortical projections. Delta rhythm is suppressed by cholinergic and noradrenergic systems. 3. A slow oscillation (< 1 Hz) is generated in the cerebral cortex and has a pivotal role in grouping the thalamic-generated sleep rhythms within wave-complexes recurring periodically, every two to five seconds. The slow rhythm is blocked by cholinergic and noradrenergic projections. Sleep rhythms consist of long-lasting inhibitory components that obliterate synaptic transmission and disconnect the brain from the outside world.

Cerebral Cortex↗

Thalamocortical oscillations in the sleeping and aroused brain.

Sleep is characterized by synchronized events in billions of synaptically coupled neurons in thalamocortical systems. The activation of a series of neuromodulatory transmitter systems during awakening blocks low-frequency oscillations, induces fast rhythms, and allows the brain to recover full responsiveness. Analysis of cortical and thalamic networks at many levels, from molecules to single neurons to large neuronal assemblies, with a variety of techniques, ranging from intracellular recordings in vivo and in vitro to computer simulations, is beginning to yield insights into the mechanisms of the generation, modulation, and function of brain oscillations.

Animals↗

The reticular thalamic nucleus projects to the contralateral dorsal thalamus in macaque monkey.

This study demonstrates, using the retrograde transport of horseradish peroxidase conjugated to the lectin wheat germ-agglutinin (WGA-HRP), that the reticular thalamic nucleus (RE) projects to the contralateral dorsal thalamus in macaque monkeys. Retrogradely labeled neurons were found in the RE nucleus following WGA-HRP injections confined to the contralateral dorsal thalamus. In light of the currently hypothesized role of the RE nucleus in the genesis of spindling rhythmicity during EEG-synchronized sleep, this findings suggests that the RE nucleus contributes to the bilateral synchrony of spindle waves through its contralateral dorsal thalamic projection.

Animals↗