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M Steriade

Publications and source records attributed to M Steriade.

At least 127 records · Page 7Linked to original sources
PubMed1991

Substantia nigra reticulata neurons during sleep-waking states: relation with ponto-geniculo-occipital waves.

We have previously hypothesized that the spike bursts of brainstem peribrachial (PB) neurons, leading to ponto-geniculo-occipital (PGO) waves in thalamocortical systems, are triggered by phasic hyperpolarizations of sufficient magnitude or by excitatory inputs reaching a steadily hyperpolarized membrane. We have proposed that the source of these hyperpolarizing actions are substantia nigra pars reticulata (SNr) cells that project to, and exert inhibitory effects upon, PB neurons. Here we tested this hypothesis by recording antidromically identified SNr-PB cells in chronically implanted, naturally sleeping cats. A subpopulation of SNr-PB cells exhibited tonically increased firing preceding by 70-200 ms the thalamic PGO wave. These data support the hypothesis that an enhancement in SNr-cells' discharges may lead to hyperpolarization of PB neurons, with the consequence of spike bursts in one class of PGO-related PB-thalamic neurons.

Animals↗
PubMed1991

Fast oscillations (20-40 Hz) in thalamocortical systems and their potentiation by mesopontine cholinergic nuclei in the cat.

Previous investigations in various motor and sensory cortical areas have shown that fast oscillations (20-80 Hz) of focal electroencephalogram and multiunit activities occur spontaneously during increased alertness or are dependent upon optimal sensory stimuli. We now report the presence of 20- to 40-Hz rhythmic activities in intracellularly recorded thalamocortical cells of the cat. In some neurons, subthreshold oscillations were triggered by depolarizing pulses and eventually gave rise to action potentials. In other neurons, the oscillations consisted of fast prepotentials, occasionally generating full spikes that arose from the resting or even from hyperpolarized membrane potential levels, and leading to trains of spikes at more depolarized levels. The rhythmic nature of these fast prepotentials was confirmed by means of an autocorrelation study, which demonstrated clear peaks at 25-ms intervals (40 Hz). In view of the recent evidence that mesopontine cholinergic nuclei trigger and maintain activation processes in thalamocortical systems, we tested the possibility that stimulation of these brainstem nuclei potentiates the 40-Hz waves on the background of the cortical electroencephalogram. This was indeed the case. The potentiation outlasted the stimulation by 10-20 s. The brainstem-induced facilitation of cortical 40-Hz oscillations was blocked by scopolamine, a muscarinic antagonist. That this facilitation was transmitted by brainstem-thalamic cholinergic projections was confirmed by persistence of the phenomenon after large excitotoxic lesions of the nucleus basalis of Meynert.

Action Potentials↗
PubMed1991

Short-lasting nicotinic and long-lasting muscarinic depolarizing responses of thalamocortical neurons to stimulation of mesopontine cholinergic nuclei.

1. The responses of thalamocortical neurons to stimulation of mesopontine [peribrachial (PB) and laterodorsal (LDT)] cholinergic nuclei were studied intracellularly in urethan-anesthetized cats. Neurons recorded from anterior thalamic (AT), ventroanterior-ventrolateral (VA-VL) and rostral intralaminar centrolateral (CL) nuclei were physiologically identified by their orthodromic responses to prethalamic stimulation and/or antidromic activation from the cerebral cortex. 2. Besides early excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) that were not sensitive to cholinergic antagonists, two types of cholinergic responses were elicited by PB/LDT stimulation: a short-lasting and a late, long-lasting depolarization. All these components survived monoamine depletion by reserpine. 3. The latency of the short-lasting depolarizing response was 147.4 +/- 27.3 (SE) ms. The response lasted for 1.3 +/- 0.1 s and had a peak amplitude of 4.2 +/- 0.3 mV. This component was associated with 10-30% increase in membrane conductance and was abolished by systemic administration of the nicotinic antagonist mecamylamine. 4. The long-lasting depolarizing response had a latency of 1.2 +/- 0.1 s, a duration of 20.8 +/- 2.2 s, and a peak amplitude of 5.4 +/- 0.4 mV. Similar values were found in decorticated animals. The duration and amplitude of the late depolarizing component were dependent on stimulation parameters and membrane potential. This response increased under depolarizing current, decreased and eventually disappeared under hyperpolarizing current, and was associated on average with 40% increase in apparent input resistance. After systemic administration of the muscarinic antagonist scopolamine, the long-lasting depolarization disappeared; the surviving short-lasting depolarization was subsequently abolished by mecamylamine. 5. The prolonged depolarizing response of thalamocortical neurons to mesopontine cholinergic stimulation was accompanied by a desynchronization of the electroencephalogram (EEG). These two phenomena had a similar time course. Stimulation of deep cerebellar nuclei, whose axons traverse the PB area, did not induce a long-lasting depolarization of target thalamic cells, nor an EEG desynchronization. 6. These data demonstrate that, in addition to an initial nicotinic excitation, brain stem cholinergic stimulation elicits a late, long-lasting muscarinic depolarization of thalamocortical neurons. We suggest that the prolonged depolarization plays an important role in cortical activation.

Animals↗
PubMed1991

Three types of inhibitory postsynaptic potentials generated by interneurons in the anterior thalamic complex of cat.

1. These experiments were carried out to study how thalamic interneurons generate inhibitory postsynaptic potentials (IPSPs) in relay cells. Intracellular recordings were performed in the anterior thalamic (AT) nuclei, a nuclear group in which interneurons constitute the only intrathalamic source of gamma-aminobutyric acid (GABA). 2. In the AT complex, as in most dorsal thalamic nuclei, interneurons can influence relay cells through their presynaptic dendrites (PSDs) and their axons. This dual mode of action is paralleled by a different termination pattern of prethalamic fibers and cortical axons on interneurons. Prethalamic fibers, which in the AT nuclei arise in the mammillary bodies (MBs), end mostly on PSDs, whereas cortical terminals usually synapse on the parent dendrites of PSDs. We therefore took advantage of the differential mode of termination of cortical and MB afferents on interneurons to infer the respective roles of the axons and PSDs of interneurons in the genesis of the IPSPs recorded from relay cells. 3. In all responsive AT cells, cortical stimuli delivered at low frequency (less than or equal to 0.5 Hz) evoked a biphasic IPSP, with an early and a late phase, having a total duration of 221.96 +/- 8.18 ms (mean +/- SE). The early part of the IPSP (termed A) had a reversal potential (ER) close to the equilibrium potential for Cl- ions: -79.25 +/- 2.14 mV. Furthermore, it reversed in polarity after impalement of the cells with KCl-filled pipettes. The late IPSP (termed B) always began before the end of the early IPSP, 45.93 +/- 2.50 ms after the onset of the A-IPSP. The B-IPSP had an ER of -109 +/- 2.4 mV and was not affected by Cl- injection. 4. By contrast, MB stimuli delivered at low frequency (less than or equal to 0.5 Hz) evoked a triphasic IPSP having a total duration of 220.5 +/- 9.42 ms in most (61.2%) AT cells. The IPSP with the shortest latency (termed a) was evoked only by MB stimuli. Before the return of the membrane potential to the resting level, a second hyperpolarizing potential began (7.41 +/- 0.46 ms after the onset of the a-IPSP). This second inhibitory phase was biphasic and had electrophysiological characteristics similar to the biphasic A- and B-IPSP evoked by cortical stimulation. Both the MB-evoked a- and A-IPSPs had an ER close to the equilibrium potential for Cl- ions (-72.22 +/- 0.68 and -72 +/- 0.82 mV, respectively) and reversed in polarity after impalement of the cells with KCl-filled pipettes.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Network modulation of a slow intrinsic oscillation of cat thalamocortical neurons implicated in sleep delta waves: cortically induced synchronization and brainstem cholinergic suppression.

A slow (0.5-4 Hz) oscillation of thalamic neurons was recently described and attributed to the interplay of two intrinsic currents. In this study, we investigated the network modulation of this intrinsic thalamic oscillation within the frequency range of EEG sleep delta-waves. We performed intracellular and extracellular recordings of antidromically identified thalamocortical cells (n = 305) in sensory, motor, associational, and intralaminar nuclei of anesthetized cats. At the resting membrane potential, Vm (-60.3 +/- 0.4 mV, mean +/- SE), cortical stimulation induced spindle-like oscillations (7-14 Hz), whereas at Vm more negative than -65 mV the same stimuli triggered an oscillation within the EEG delta-frequency (0.5-4 Hz), consisting of low-threshold spikes (LTSs) followed by after hyperpolarizing potentials (AHPs). The LTS-AHP sequences outlasted cortical stimuli as a self-sustained rhythmicity at 1-2 Hz. Corticothalamic stimuli were able to transform subthreshold slow (0.5-4 Hz) oscillations, occurring spontaneously at Vm more negative than -65 mV, into rhythmic LTSs crowned by bursts of Na+ spikes that persisted for 10-20 sec after cessation of cortical volleys. Cortical volleys also revived a hyperpolarization-activated slow oscillation when it dampened after a few cycles. Auto- and crosscorrelograms of neuronal pairs revealed that unrelated cells became synchronized after a series of corticothalamic stimuli, with both neurons displaying rhythmic (1-2 Hz) bursts or spike trains. Since delta-thalamic oscillations, prevailing during late sleep stages, are triggered at more negative Vm than spindles characterizing the early sleep stage, we postulate a progressive hyperpolarization of thalamocortical neurons with the deepening of the behavioral state of EEG-synchronized sleep. In view of the evidence that cortical-elicited slow oscillations depend on synaptically induced hyperpolarization of thalamocortical cells, we propose that the potentiating influence of the corticothalamic input results from the engagement of two GABAergic thalamic cell classes, reticular and local-circuit neurons. The thalamocorticothalamic loop would transfer the spike bursts of thalamic oscillating cells to cortical targets, which in turn would reinforce the oscillation by direct pathways and/or indirect projections relayed by reticular and local-circuit thalamic cells. Stimulation of mesopontine cholinergic [peribrachial (PB) and laterodorsal tegmental (LDT)] nuclei in monoamine-depleted animals had an effect that was opposite to that exerted by corticothalamic volleys. PB/LDT stimulation reduced or suppressed the slow (1-4 Hz) oscillatory bursts of high-frequency spikes in thalamic cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1990

Substantia nigra pars reticulata projects to the reticular thalamic nucleus of the cat: a morphological and electrophysiological study.

The projections of substantia nigra pars reticulata (SNr) toward the reticular (RE) thalamic complex of cat were studied morphologically and electrophysiologically. Numerous SNr cells were retrogradely labeled following injections of horseradish peroxidase conjugated to wheat-germ agglutinin (WGA-HRP) in the rostral and rostrolateral part of the RE thalamic nucleus. Iontophoretic injections of Phaseolus vulgaris leucoagglutinin (PHA-L) in the SNr confirmed that this retrograde labeling was not a consequence of tracer diffusion in neighboring structures, but reflected a genuine SNr projection to the RE thalamic nucleus. Indeed, widely branched and varicose PHA-L-positive fibers were found in the rostral and rostrolateral pole of the RE thalamic nucleus following PHA-L injections in the SNr. Furthermore, in agreement with previous data indicating that nigrothalamic cells are GABAergic, electrical stimulation of the SNr evoked a short-latency inhibitory effect acting on both spontaneous and cortically-evoked discharges of most RE thalamic neurons. These results are discussed in light of the possible role of the SNr and RE thalamic complex in attentional processes.

Action Potentials↗
PubMed1990

Brainstem genesis of reserpine-induced ponto-geniculo-occipital waves: an electrophysiological and morphological investigation.

Several experimental results indicate that the peribrachial (PB) cholinergic area of the pedunculopontine nucleus is the final relay for the transfer of brainstem-generated pontogeniculo-occipital (PGO) waves to the thalamus. However, the mechanisms underlying the PGO-related activity of PB neurons remain unknown. In order to study these mechanisms, single unit recordings in the PB area were performed in reserpinized cats. Because PGO waves are closely related to rapid eye movements, our microelectrode explorations were also aimed to some structures of the preoculomotor network, namely, the superior colliculus (SC) and parts of the central tegmental field (FTC). We have found several classes of PGO-on cells in the PB area, most of them descharging 80 ms or less before the peak of PGO waves. These cell-classes comprised high-frequency bursting cells, slow-frequency bursting cells, and neurons discharging single spikes or doublets. Intracellular recordings showed that PGO-on single spikes arise from conventional excitatory postsynaptic potentials. Among PGO-related cells in structures outside the PB limits, it was found that most SC cells discharge during or after the PGO, whereas FTC cells increase their discharge rate several hundreds of ms before PGO waves, thus indicating that PGO waves are elaborated long before the activation of PB neurons. Massive retrograde labeling was found in FTC following horseradish peroxidase injections into the PB area. We suggest that long-lead FTC neurons provide an excitatory input to PGO-on PB neurons.

Animals↗
PubMed1990

Different cellular types in mesopontine cholinergic nuclei related to ponto-geniculo-occipital waves.

The only mesopontine neurons previously described as involved in the transfer of ponto-geniculo-occipital (PGO) waves from the brain stem to the thalamus were termed PGO-on bursting cells. We have studied, in chronically implanted cats, neuronal activities in brain-stem peribrachial (PB) and laterodorsal tegmental (LDT) cholinergic nuclei in relation to PGO waves recorded from the lateral geniculate (LG) thalamic nucleus during rapid-eye-movement (REM) sleep. We constructed peri-PGO histograms of PB/LDT cells' discharges and analyzed the interspike interval distribution during the period of increased neuronal activity related to PGO waves. Six categories of PGO-related PB/LDT neurons with identified thalamic projections were found: 4 classes of PGO-on cells: PGO-off but REM-on cells: and post-PGO cells. The physiological characteristics of a given cell class were stable even during prolonged recordings. One of these cell classes (1) represents the previously described PGO-on bursting neurons, while the other five (2-6) are newly discovered neuronal types. (1) Some neurons (16% of PGO-related cells) discharged stereotyped low-frequency (120-180 Hz) spike bursts preceding the negative peak of the LG-PGO waves by 20-40 msec. These neurons had low firing rates (0.5-3.5 Hz) during all states. (2) A distinct cell class (22% of PGO-related neurons) fired high-frequency spike bursts (greater than 500 Hz) about 20-40 msec prior to the thalamic PGO wave. These bursts were preceded by a period (150-200 msec) of discharge acceleration on a background of tonically increased activity during REM sleep. (3) PGO-on tonic neurons (20% of PGO-related neurons) discharged trains of repetitive single spikes preceding the thalamic PGO waves by 100-150 msec, but never fired high-frequency spike bursts. (4) Other PGO-on neurons (10% of PGO-related neurons) discharged single spikes preceding thalamic PGO waves by 15-30 msec. On the basis of parallel intracellular recordings in acutely prepared, reserpine-treated animals, we concluded that the PGO-on single spikes arise from conventional excitatory postsynaptic potentials and do not reflect tiny postinhibitory rebounds. (5) A peculiar cellular class, termed PGO-off elements (8% of PGO-related neurons), consisted of neurons with tonic, high discharge rates (greater than 30 Hz) during REM sleep. These neurons stopped firing 100-200 msec before and during the thalamic PGO waves. (6) Finally, other neurons discharged spike bursts or tonic spike trains 100-300 msec after the initially negative peak of the thalamic PGO field potential (post-PGO elements, 23% of PGO-related neurons).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Prolonged enhancement of anterior thalamic synaptic responsiveness by stimulation of a brain-stem cholinergic group.

This study describes the effects of brain-stem cholinergic laterodorsal tegmental (LDT) stimulation on the synaptic responsiveness of anterior thalamic (AT) neurons. A sample of AT cells, physiologically identified by their short-latency (less than 6.5 msec) response to mammillary body (MB) stimulation, was recorded in unanesthetized, chronically implanted cats and in urethane-anesthetized cats. In chronic experiments, LDT stimulation evoked a short-latency (10-20 msec) excitation in most AT cells. Moreover, brief LDT trains (3 shocks at 300 Hz, every 3 sec) enhanced the responsiveness of AT cells to both MB (orthodromic) and cortical (ortho- and antidromic) stimuli. This effect did not vary as a function of the interval between LDT conditioning and MB or cortical testing shocks, but as a function of the number of trials. The effects of LDT stimuli resisted reserpine treatment (0.75 mg/kg), suggesting that they were not dependent on the coactivation of monoaminergic fibers. Finally, LDT trains did not suppress inhibitory processes in AT neurons when conditioning-testing intervals were longer than 60 msec. Intracellular recordings performed in urethane-anesthetized cats revealed that LDT stimulation induced a short-latency depolarization which increased with membrane hyperpolarization and was associated with an increase in apparent membrane conductance. Usually, isolated LDT trains did not evoke lasting changes in membrane potential or conductance. However, when LDT trains were applied every 3 sec, they gradually decreased the apparent membrane conductance without altering the membrane potential. This conductance change had a time course similar to the LDT-induced potentiation of responsiveness observed in the chronic experiments. In some neurons, LDT conditioning trains also induced a marked increase in the probability of fast prepotentials being triggered by subthreshold MB or cortical orthodromic volleys. In order to distinguish the cumulative effects of repeated LDT trains from the possibly slow time course of LDT influences, we studied the effects of a unique 1 sec LDT train (at 30 Hz) on the synaptic responsiveness of AT cells recorded extracellularly in reserpine-treated, urethane-anesthetized animals. Such LDT trains induced a 2.9-fold increase in synaptic responsiveness, reaching its peak 40-50 sec after the LDT train and lasting up to 4 min. Iontophoretic application of the muscarinic blocker scopolamine blocked these long-lasting potentiating effects of LDT stimuli. Removal of cortical and basal forebrain inputs to the AT nuclear complex by appropriate transections did not abolish the potentiating effects of LDT trains.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Neuronal activities in brain-stem cholinergic nuclei related to tonic activation processes in thalamocortical systems.

This study was performed to examine the hypothesis that thalamic-projecting neurons of mesopontine cholinergic nuclei display activity patterns that are compatible with their role in inducing and maintaining activation processes in thalamocortical systems during the states of waking (W) and rapid-eye-movement (REM) sleep associated with desynchronization of the electroencephalogram (EEG). A sample of 780 neurons located in the peribrachial (PB) area of the pedunculopontine tegmental nucleus and in the laterodorsal tegmental (LDT) nucleus were recorded extracellularly in unanesthetized, chronically implanted cats. Of those neurons, 82 were antidromically invaded from medial, intralaminar, and lateral thalamic nuclei: 570 were orthodromically driven at short latencies from various thalamic sites: and 45 of the latter elements are also part of the 82 cell group, as they were activated both antidromically and synaptically from the thalamus. There were no statistically significant differences between firing rates in the PB and LDT neuronal samples. Rate analyses in 2 distinct groups of PB/LDT neurons, with fast (greater than 10 Hz) and slow (less than 2 Hz) discharge rates in W, indicated that (1) the fast-discharging cell group had higher firing rates in W and REM sleep compared to EEG-synchronized sleep (S), the differences between all states being significant (p less than 0.0005); (2) the slow-discharging cell group increased firing rates from W to S and further to REM sleep, with significant difference between W and S (p less than 0.01), as well as between W or S and REM sleep (p less than 0.0005). Interspike interval histograms of PB and LDT neurons showed that 75% of them have tonic firing patterns, with virtually no high-frequency spike bursts in any state of the wake-sleep cycle. We found 22 PB cells that discharged rhythmic spike trains with recurring periods of 0.8-1 sec. Autocorrelograms revealed that this oscillatory behavior disappeared when their firing rate increased during REM sleep. Dynamic analyses of sequential firing rates throughout the waking-sleep cycle showed that none of the full-blown states of vigilance is associated with a uniform level of spontaneous firing rate. Signs of decreased discharge frequencies of mesopontine neurons appeared toward the end of quiet W, preceding by about 10-20 sec the most precocious signs of EEG synchronization heralding the sleep onset. During transition from S to W, rates of spontaneous discharges increased 20 sec before the onset of EEG desynchronization.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Neuronal activity of identified posterior hypothalamic neurons projecting to the brainstem peribrachial area of the cat.

Following horseradish peroxidase injections in the brainstem peribrachial (PB) area, massive retrograde labeling was found in the posterior hypothalamic region. Single-unit recordings posterior hypothalamic neurons with antidromically identified projections to the PB area revealed that these neurons have higher firing rates in waking than in slow-wave sleep and dissimilar discharge patterns as compared with intralaminar thalamic neurons. The results are discussed in the context of reciprocal hypothalamo-brainstem circuits.

Action Potentials↗
PubMed1989

The effects of brainstem peribrachial stimulation on perigeniculate neurons: the blockage of spindle waves.

The mode of action of afferents arising from the brainstem peribrachial region at the midbrain-pontine junction on neurons recorded from the reticular thalamic sector adjacent to the lateral geniculate nucleus (perigeniculate cells) was investigated at the intracellular level in the cat. Experiments were performed in cats under barbiturate or urethane anaesthesia and in non-anaesthetized deafferented animals. Most cats were pretreated with reserpine (1-2 mg/kg) and were also acutely deprived of their retinal and cortical visual inputs. It was found that peribrachial stimulation produced a short train of fast-rising depolarizations followed by a long-lasting period of hyperpolarization in all perigeniculate neurons. Although the latest part of the early depolarizations preceding the hyperpolarization resulted from a parallel activation of lateral geniculate relay neurons by peribrachial afferents, those occurring at shortest latencies appear to result from a direct excitation produced by peribrachial afferents. Furthermore, these early excitatory postsynaptic potentials persisted under deep barbiturate anaesthesia, a condition that prevents activation of thalamic relay neurons by peribrachial stimulation. The evoked hyperpolarization decreased with membrane hyperpolarization, was associated with a 40-50% increase in membrane conductance and was insensitive to Cl injections. It was no longer observed within one hour after i.v. injection of scopolamine. However, the depolarizing responses were not depressed by this muscarinic antagonist. Iontophoretic applications of scopolamine also removed peribrachial-evoked inhibition of synaptic responses triggered by optic chiasma stimulation. The peribrachial input exerted a powerful control on the oscillatory behavior of perigeniculate neurons. Spindle oscillations which are generated within the reticular thalamic complex were readily blocked by peribrachial stimulation. It is then concluded that the transition from an oscillatory to a relay mode of operation in the thalamus is controlled at least in part by a muscarinic inhibition of reticular thalamic neurons. The synaptic mechanism responsible for the early depolarization remains to be elucidated.

Action Potentials↗
PubMed1989

The effects of brainstem peribrachial stimulation on neurons of the lateral geniculate nucleus.

The intracellular effects of brainstem peribrachial stimulation on lateral geniculate neurons were investigated in the cat. Experiments were performed in cats under barbiturate or urethane anaesthesia and in non-anaesthetized deafferented animals. Most animals were pretreated with reserpine and were acutely deprived of their retinal and visual cortical inputs. Short trains of stimuli triggered a transient depolarization in most relay neurons (latency: 20-30 ms; duration: 200-300 ms). This depolarization could be interrupted by a short-duration unitary inhibitory postsynaptic potential. The depolarization increased with membrane hyperpolarization and was associated with an increase in membrane conductance. The inhibitory postsynaptic potential had an intrathalamic origin and likely resulted from parallel activation of intrageniculate interneurons. The above responses were largely enhanced in reserpinized cats and were completely abolished by small doses of barbiturates. Iontophoretic applications of the nicotinic blocker, hexamethonium, eliminated peribrachial-evoked discharges in these cells, while similar applications of the muscarinic antagonist, scopolamine, were devoid of any effect. The conclusion is reached that the depolarization of lateral geniculate relay neurons by peribrachial afferents represents a direct postsynaptic effect and does not result from a global disinhibitory mechanism involving inhibition of perigeniculate cells and intrageniculate interneurons. This peribrachial-evoked transient excitation of relay neurons results from a nicotinic mechanism.

Action Potentials↗
PubMed1989

The cellular mechanism of thalamic ponto-geniculo-occipital waves.

The cellular mechanisms underlying the genesis of thalamic ponto-geniculo-occipital waves were studied in reserpinized cats under urethane anaesthesia. Simultaneous field potential and intracellular recordings were performed in the lateral geniculate nucleus after acute lesions of retinal and visual cortical inputs. In most relay cells, reserpine-induced ponto-geniculo-occipital waves were associated with a transient depolarization that was often interrupted by a unitary inhibitory postsynaptic potential. The depolarization grew in size with membrane hyperpolarization and was accompanied by an increase in membrane conductance. The inhibitory postsynaptic potential is likely to have resulted from the activation of intrageniculate interneurons since perigeniculate cells were always inhibited during the occurrence of ponto-geniculo-occipital waves. Under reserpine, thalamic ponto-geniculo-occipital waves could also be triggered by peribrachial or auditory stimulation. These evoked ponto-geniculo-occipital waves were associated with intracellular events identical to those occurring spontaneously after reserpine administration. In addition, thalamic spindle oscillations were readily blocked by the occurrence of spontaneous or evoked ponto-geniculo-occipital waves. On the basis of the present results and those already published in the literature, the conclusion is reached that lateral geniculate ponto-geniculo-occipital waves result from a nicotinic activation of relay cells and from a parallel muscarinic inhibition of perigeniculate cells by peribrachial afferents. The functional significance of the ponto-geniculo-occipital activity is discussed on the basis of the antagonistic action of these signals on thalamic oscillations. It is proposed that these signals are the central correlates of orienting reactions elicited by sensory stimuli during waking (the so-called eye movement potentials) and by internally generated drives during paradoxical sleep.

Action Potentials↗
PubMed1989

Phasic activation of lateral geniculate and perigeniculate thalamic neurons during sleep with ponto-geniculo-occipital waves.

Ponto-geniculo-occipital (PGO) waves are spiky field potentials generated in cholinergic nuclei of the dorsolateral mesopontine tegmentum just prior to and during rapid-eye-movement (REM) sleep and transferred toward thalamic nuclei. These events are commonly regarded as physiological correlates of oneiric behavior. We have examined the PGO-related discharges of physiologically identified neurons located in the dorsal lateral geniculate (LG) nucleus and perigeniculate (PG) sector of the reticular thalamic complex in chronically implanted, naturally sleeping cats. PGO focal waves and associated unit discharges were simultaneously recorded by the same microelectrode. PGO waves herald the other signs of REM sleep (EEG desynchronization and muscular atonia), appearing 30-90 sec before REM sleep over the EEG-synchronized activity of slow-wave sleep (pre-REM epoch). (1) Most PG neurons discharged bursts of action potentials in relation to PGO waves during both pre-REM and REM sleep. (2) The PGO-related activity of LG neurons was quite different. During the pre-REM stage, PGO waves correlated with a short (7-15 msec), high-frequency (300-500 Hz) spike burst of LG neurons, followed by a long (0.2-0.4 sec) train of single spikes, whereas during REM sleep, the PGO-related activity lacked the initial burst and consisted of a spike train that only slightly exceeded the tonically increased background firing of LG cells. The stereotyped characteristics of the PGO-related spike bursts during the pre-REM epoch suggest that they are the extracellular reflection of a low-threshold spike deinactivated by the tonic membrane hyperpolarization of LG cells associated with the EEG-synchronized sleep state. Such bursts are inactivated during the tonic depolarization of LG cells that occurs in REM sleep. The synchronous spike bursts discharged by LG cells in relation with the PGO waves of the pre-REM epoch probably underlie the much larger amplitude of the PGO waves of the pre-REM epoch as compared with those of the REM-sleep state. Since LG neurons have relatively low spontaneous firing rates during the EEG-synchronized pre-REM epoch, the PGO-related activity of this transitional stage leads to a higher signal-to-noise ratio in the visual thalamocortical channel than during REM sleep. We suggest that the PGO-related activity during the pre-REM epoch is related to vivid imagery during this stage of sleep.

Animals↗