The hypothesis that nucleus reticularis thalami (RE) is the generator of spindle rhythmicity during electroencephalogram (EEG) synchronization was tested in acutely prepared cats. Unit discharges and focal waves were extracellularly recorded in the rostral pole of RE nucleus, which was completely disconnected by transections from all other thalamic nuclei. In some experiments, additional transections through corona radiata created a triangular island in which the rostral RE pole survived with the caudate nucleus, putamen, basal forebrain nuclei, prepyriform area, and the adjacent cortex. Similar results were obtained in two types of experiments: brain stem-transected preparations that exhibited spontaneous spindle sequences, and animals under ketamine anesthesia in which transient spindling was repeatedly precipitated during recording by very low doses of a short-acting barbiturate. Both spindle-related rhythms (7- to 16-Hz waves grouped in sequences that recur with a rhythm of 0.1-0.3 Hz) are seen in focal recordings of the deafferented RE nucleus. The presence of spindling rhythmicity in the disconnected RE nucleus contrasts with total absence of spindles in cortical EEG leads and in thalamic recordings behind the transection. Oscillations within the same frequency range as that of spontaneous spindles can be evoked in the deafferented RE nucleus by subcortical white matter stimulation. In deafferented RE cells, the burst structure consists of an initially biphasic acceleration-deceleration pattern, eventually leading to a long-lasting tonic tail. Quantitative group data show that the burst parameters of disconnected RE cells are very similar to those of RE neurons with intact connections. In the deafferented RE nucleus, spike bursts of RE neurons recur periodically (0.1-0.3 Hz) in close time-relation with simultaneously recorded focal spindle sequences. The burst occurrence of deafferented RE cells is greatly reduced after systemic administration of bicuculline. The preservation of both spindle-related rhythms in the disconnected RE nucleus, together with our recent experiments showing abolition of spindle oscillations in thalamic nuclei after lesions of RE nucleus (24), demonstrate that RE nucleus is the generator of spindle rhythms.
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)
This study tested the hypothesis that inhibitory actions are exerted by reticularis thalami (RE) neurons upon thalamocortical neurons. The RE neurons were recorded in the rostral pole and lateral districts of the nucleus, and were activated monosynaptically by cortical volleys. Thalamocortical neurons were identified antidromically in intralaminar and ventrolateral nuclei. During sleep with EEG synchronization, prolonged spike barrages of RE neurons extended over the whole spindle sequences. This result suggests that RE neurons are depolarized throughout spindle oscillations, whereas thalamocortical neurons show, simultaneously, long hyperpolarizations and short rebounds. During waking, parallelism rather than reciprocity was found between RE and thalamocortical neurons. Spontaneous discharge rates almost doubled in RE neurons on arousal from sleep, and the probability of cortically evoked short-latency discharges increased. The increase in spontaneous firing rates of RE neurons during natural arousal is consistent with their short-latency synaptic excitation by stimulating the rostral brain stem reticular formation after chronic degeneration of passing fibers. We suggest that RE cells inhibit GABAergic local-circuit cells, in addition to inhibiting thalamocortical neurons, and that different ratios of inhibitory effects are exerted by RE neurons upon these two cell classes during waking and sleep. We further suggest that, upon arousal, disinhibition of thalamocortical neurons (via the local-circuit neurons) outweighs direct inhibition of the thalamocortical neurons.
Previous investigations in various motor and sensory cortical areas have shown that fast oscillations 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 ofthese fast prepotgntials was confimed 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. 4396The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
SUMMARY1. Unit discharges were extracellularly recorded from antidromically identified thalamocortical neurones of ventralis lateralis (v.1.) and centralis lateralis (c.l.) nuclei as well as from reticularis thalami (re.) neurones during wakefulness and electroencephalogram-synchronized sleep of the behaving cat. Various parameters of sleep-related discharge bursts were analysed.2. Statistical analyses revealed striking similarities between motor relay (v.1.) and intralaminar (c.l.) neurones. More than 60 % of bursts consist of three to five spikes at 250-400 Hz. The defining feature of bursts in all cortically projecting neurones is a progressive increase in the duration of successive interspike intervals. 3. As in thalamocortical cells, all re. neurones change their tonic discharges in waking to bursting firing in sleep, regardless of the increased or decreased firing rates from wake to sleep in individual neurones. The bursts of re. neurones are essentially different from those of thalamocortical cells. In re. neurones, burst structure consists of an initial progressive decrease in duration of interspike intervals, followed by an increase in duration of successive intervals, eventually leading to a long-lasting tonic spike train at about 100 Hz. In contrast with bursts of thalamocortical neurones, only 6 % of re. bursts are shorter than 50 ms; the total duration of the burst extends between 50 ms and 1'5 s. Population periburst histograms show the beginning of a decline in firing probability about 1-5 s prior -to burst onset and an increased firing probability persisting for 300-350 ms after burst onset.4. The different electrophysiological properties underlying the burst structure of cat's thalamocortical and re. neurones are discussed, with emphasis on dissimilar aspects of re. bursts in unanaesthetized and barbituratized preparations. Various factors that may account for the transition from tonic mode in waking to bursting mode in sleep are envisaged.
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