Neuronal Synchrony during Anesthesia: A Thalamocortical Model (original) (raw)
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Synchronization of low-frequency rhythms in corticothalamic networks
1997
We have investigated the degree of synchronization between cortical, thalamic reticular and thalamocortical neurons of cats during low-frequency (<15 Hz) sleep-like oscillations, as they appear under anaesthesia. We have also studied the effects exerted by cortical stimulation on the synchronization among thalamic units. Parallel experiments [Steriade et al. (1996) J. Neurosci. 16, 392-417] in this laboratory have demonstrated the similarity between the slow oscillation (<1 Hz) under ketamine-xylazine anaesthesia and that occurring during the natural state of resting sleep. Spontaneous activity was recorded simultaneously, with independent microelectrodes, from groups of two to five physiologically identified neurons. The rhythmicity of spontaneous activity and the temporal relations between cellular discharges were statistically evaluated by auto-and crosscorrelation techniques. We have found no topography in the distribution of synchronization between thalamic reticular and thalamocortical cells. Only the slow, cortical-generated oscillation (<1 Hz) displayed a stable frequency and correlation among groups of cortical and thalamic cells. The other two sleep oscillations (thalamic-generated spindles at 7-14 Hz and clock-like delta at 1-4 Hz) fluctuated in frequency and the degree of correlation between neurons varied. Cortical volleys entrained and synchronized thalamic cells, and triggered synchronized spindling in the thalamus.
Thalamocortical synchronization during induction and emergence from propofol-induced unconsciousness
Proceedings of the National Academy of Sciences of the United States of America, 2017
General anesthesia (GA) is a reversible drug-induced state of altered arousal required for more than 60,000 surgical procedures each day in the United States alone. Sedation and unconsciousness under GA are associated with stereotyped electrophysiological oscillations that are thought to reflect profound disruptions of activity in neuronal circuits that mediate awareness and cognition. Computational models make specific predictions about the role of the cortex and thalamus in these oscillations. In this paper, we provide in vivo evidence in rats that alpha oscillations (10-15 Hz) induced by the commonly used anesthetic drug propofol are synchronized between the thalamus and the medial prefrontal cortex. We also show that at deep levels of unconsciousness where movement ceases, coherent thalamocortical delta oscillations (1-5 Hz) develop, distinct from concurrent slow oscillations (0.1-1 Hz). The structure of these oscillations in both cortex and thalamus closely parallel those obser...
A Thalamacortical Feedback Model to Explain EEG During Anesthesia
Understanding Complex Systems, 2015
General anesthesia (GA) is a medical procedure which aims to achieve unconsciousness, analgesia, amnesia, and immobility. Although GA is commonly used in medical care for patients undergoing surgery, its precise underlying mechanisms and the molecular action of anesthetic agents (AA) remain to be elucidated. A wide variety of drugs are used in modern anesthetic practice and it has been observed that for many AAs, during the transition from consciousness to unconsciousness, the electroencephalogram shows biphasic effects in amplitude: an initial increase of the spectral power followed by a decrease at higher concentrations. Moreover during the administration of propofol, specific changes in EEG rhythms can be observed. The aim of this work is the extended discussion of a recent model by Hindriks and van Putten [8] that reproduces specific changes in EEG rhythms by the study of a neuronal population model of a single thalamocortical module. We illustrate specific features of the model, such as the physiological assumptions, the derivation of the power spectral density and the impact of the propofol concentration and of the stationary state. We show that the propofol-induced modification of the stationary state plays an important role in the understanding of the observed EEG.
State-dependent fluctuations of low-frequency rhythms in corticothalamic networks
1997
We have studied the variations in the degree of correlated firing within the low-frequency sleep rhythms (<15 Hz) between cortical, thalamic reticular and thalamocortical neurons during changes in the amplitude and frequency of brain electrical activity in anaesthetized cats. Extracellular discharges of neuronal groups of two to five physiologically identified cortical and thalamic units were recorded simultaneously with independent microelectrodes. The firing patterns and the temporal correlation between spike-trains were evaluated by auto-and crosscorrelograms. Although the animals were under deep anaesthesia, additional doses of the same or different anaesthetics were able to alter the electroencephalographic pattern, inducing waves with higher amplitude. Similar transitions occurred spontaneously. We found that the presence of rhythmic behaviour in cells of corticothalamic networks, as well as their degree of correlated firing, was extremely sensitive to even slight alterations in the state of the electroencephalogram. Cells belonging to the same functional system, but located distantly, became highly synchronized upon the increased amplitude of brain waves.
Thalamocortical model for a propofol-induced -rhythm associated with loss of consciousness
Proceedings of the National Academy of Sciences, 2010
Recent data reveal that the general anesthetic propofol gives rise to a frontal α-rhythm at dose levels sufficient to induce loss of consciousness. In this work, a computational model is developed that suggests the network mechanisms responsible for such a rhythm. It is shown that propofol can alter the dynamics in thalamocortical loops, leading to persistent and synchronous α-activity. The synchrony that forms in the cortex by virtue of the involvement of the thalamus may impede responsiveness to external stimuli, thus providing a correlate for the unconscious state.
Altered temporal variance and neural synchronization of spontaneous brain activity in anesthesia
Human brain mapping, 2014
Recent studies at the cellular and regional levels have pointed out the multifaceted importance of neural synchronization and temporal variance of neural activity. For example, neural synchronization and temporal variance has been shown by us to be altered in patients in the vegetative state (VS). This finding nonetheless leaves open the question of whether these abnormalities are specific to VS or rather more generally related to the absence of consciousness. The aim of our study was to investigate the changes of inter- and intra-regional neural synchronization and temporal variance of resting state activity in anesthetic-induced unconsciousness state. Applying an intra-subject design, we compared resting state activity in functional magnetic resonance imaging (fMRI) between awake versus anesthetized states in the same subjects. Replicating previous studies, we observed reduced functional connectivity within the default mode network (DMN) and thalamocortical network in the anesthet...
F1000 - Post-publication peer review of the biomedical literature, 2017
General anesthesia (GA) is a reversible drug-induced state of altered arousal required for more than 60,000 surgical procedures each day in the United States alone. Sedation and unconsciousness under GA are associated with stereotyped electrophysiological oscillations that are thought to reflect profound disruptions of activity in neuronal circuits that mediate awareness and cognition. Computational models make specific predictions about the role of the cortex and thalamus in these oscillations. In this paper, we provide in vivo evidence in rats that alpha oscillations (10-15 Hz) induced by the commonly used anesthetic drug propofol are synchronized between the thalamus and the medial prefrontal cortex. We also show that at deep levels of unconsciousness where movement ceases, coherent thalamocortical delta oscillations (1-5 Hz) develop, distinct from concurrent slow oscillations (0.1-1 Hz). The structure of these oscillations in both cortex and thalamus closely parallel those observed in the human electroencephalogram during propofol-induced unconsciousness. During emergence from GA, this synchronized activity dissipates in a sequence different from that observed during loss of consciousness. A possible explanation is that recovery from anesthesiainduced unconsciousness follows a "boot-up" sequence actively driven by ascending arousal centers. The involvement of medial prefrontal cortex suggests that when these oscillations (alpha, delta, slow) are observed in humans, self-awareness and internal consciousness would be impaired if not abolished. These studies advance our understanding of anesthesia-induced unconsciousness and altered arousal and further establish principled neurophysiological markers of these states. anesthesia | prefrontal cortex | thalamus | coherence | propofol G eneral anesthesia (GA) is a reversible drug-induced state consisting of unconsciousness, analgesia, amnesia, akinesia, and physiological stability (1). In the United States nearly 60,000 surgical procedures are conducted under GA every day, making GA one of the most common manipulations of the brain and central nervous system in medicine (1). The molecular mechanisms by which anesthetic drugs alter brain function have been well characterized (2, 3). Detailed analyses of neural circuitand systems-level mechanisms of GA are more recent (1, 4, 5). Understanding the system-wide effects of anesthetic drugs is necessary in order to understand how these drugs produce states of altered arousal and unconsciousness. One of the most commonly used anesthetic drugs is 2,6diisopropylphenol (propofol), a GABA-A receptor agonist (6). Electroencephalogram (EEG) recordings in humans during gradual induction of unconsciousness with propofol show the appearance of frontal β oscillations (15-30 Hz) at the onset of sedation, followed by the appearance of coherent frontal α (8-12 Hz) oscillations (7-10) and widespread slow (0.1-1 Hz) and δ (1-4 Hz) oscillations (7, 11, 12) when subjects no longer respond to sensory stimuli. Biophysical models of neuronal dynamics have shown that whereas α and β oscillations can be generated by propofol's actions in cortex alone (13), coherent α
Frontiers in Pharmacology
Background: Electroencephalography (EEG) recordings under propofol exhibit an increase in slow and alpha oscillation power and dose-dependent phase–amplitude coupling (PAC), which underlie GABAA potentiation and the central role of thalamocortical entrainment. However, the exact EEG signatures elicited by volatile anesthetics and the possible neurophysiological mechanisms remain unclear.Methods: Cortical EEG signals and thalamic local field potential (LFP) were recorded in a mouse model to detect EEG signatures induced by 0.9%, 1.5%, and 2.0% isoflurane. Then, the power of the EEG spectrum, thalamocortical coherence, and slow–alpha phase–amplitude coupling were analyzed. A computational model based on the thalamic network was used to determine the primary neurophysiological mechanisms of alpha spiking of thalamocortical neurons under isoflurane anesthesia.Results: Isoflurane at 0.9% (light anesthesia) increased the power of slow and delta oscillations both in cortical EEG and in tha...
2014
How general anesthetics cause loss of consciousness is unknown. Some evidence points toward effects on the neocortex causing "topdown" inhibition, whereas other findings suggest that these drugs act via subcortical mechanisms, possibly selectively stimulating networks promoting natural sleep. To determine whether some neuronal circuits are affected before others, we used Morlet wavelet analysis to obtain high temporal resolution in the time-varying power spectra of local field potentials recorded simultaneously in discrete brain regions at natural sleep onset and during anesthetic-induced loss of righting reflex in rats. Although we observed changes in the local field potentials that were anesthetic-specific, there were some common changes in high-frequency (20-40 Hz) oscillations (reductions in frequency and increases in power) that could be detected at, or before, sleep onset and anesthetic-induced loss of righting reflex. For propofol and natural sleep, these changes occur first in the thalamus before changes could be detected in the neocortex. With dexmedetomidine, the changes occurred simultaneously in the thalamus and neocortex. In addition, the phase relationships between the low-frequency (1-4 Hz) oscillations in thalamic nuclei and neocortical areas are essentially the same for natural sleep and following dexmedetomidine administration, but a sudden change in phase, attributable to an effect in the central medial thalamus, occurs at the point of dexmedetomidine loss of righting reflex. Our data are consistent with the central medial thalamus acting as a key hub through which general anesthesia and natural sleep are initiated.