Intracellular analysis of relations between the slow (< 1 Hz) neocortical oscillation and other sleep rhythms of the electroencephalogram

Abstract

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)

Mesoscale infraslow spontaneous membrane potential fluctuations recapitulate high-frequency activity cortical motifs

“…2). A broad local peak in the power spectra indicated oscillatory activity associated with the slow oscillation (1 Hz) 34,37 and delta oscillation (1.5-4 Hz), which predominate under anaesthesia and natural sleep and can be observed in states of quiet wakefulness 27,33,34 . As in our DC-EEG and LFP recordings of spontaneous activity, we observe the presence of substantial power in the infraslow frequency (o0.1 Hz) range indicating a significant presence of infraslow spontaneous activity in our cortical VSD signals ( Supplementary Fig.…”

Integrated Brain Circuits: Neuron-Astrocyte Interaction in Sleep-Related Rhythmogenesis

“…Pioneering work by Steriade and colleagues has shown that identified neurons in a number of different cortical areas fluctuate between depolarized (UP) and hyperpolarized (DOWN) states[29,30,31]. The UP state is characterized by barrages of synaptic activity, a plateau depolarization, and action potential firing, while the DOWN state is characterized by cell hyperpolarization and silence[30] (Fig.…”

“…Interestingly, although the isolated cortical slices and cortical slabs can generate slow oscillations independently of the thalamus[30,47,50,51], there has been no formal quantitative analysis of the characteristics of cortical slow oscillations in the absence of the thalamus[52]. A recently proposed view of the slow oscillation suggests that this rhythm is generated by a synaptic-based cortical oscillator and two intrinsic thalamic oscillators: thalamocortical neurons and neurons of the TRN[52].…”

“…In SWS, the thalamocortical system is dominated by stereotyped field potential oscillations in the 0.5- to 4-Hz frequency range, which includes the slow (<1 Hz) oscillation and delta frequencies (1–4 Hz). Analytically described by Steriade and colleagues 17 years ago[29,30,31], the slow oscillation is now thought to be one of the primary organizers of network activity in the thalamocortical system[32] and possibly the key player in off-line memory consolidation during sleep[10,21,26]. In the remainder of this review, we will first discuss the neuronal mechanisms underlying slow oscillations, highlighting the role of dynamic cortico- and thalamocortical coupling to generate this network activity.…”

Microwave effects on the nervous system

“…There is further doubt that the effect can be a result of a high susceptibility of subcortical structures such as the thalamus since sleep spindles can be generated in the cortex alone [Steriade et al, 1993]. Their 87% duty cycle versus the usual GSM digital phone cycle of 12.5% may be a factor.…”