Neural Correlates of Wakefulness, Sleep, and General Anesthesia

Abstract

Background Significant advances have been made in our understanding of subcortical processes related to anesthetic- and sleep-induced unconsciousness, but the associated changes in cortical connectivity and cortical neurochemistry have yet to be fully clarified. Methods Male Sprague–Dawley rats were instrumented for simultaneous measurement of cortical acetylcholine and electroencephalographic indices of corticocortical connectivity—coherence and symbolic transfer entropy—before, during, and after general anesthesia (propofol, n = 11; sevoflurane, n = 13). In another group of rats (n = 7), these electroencephalographic indices were analyzed during wakefulness, slow wave sleep (SWS), and rapid eye movement (REM) sleep. Results Compared to wakefulness, anesthetic-induced unconsciousness was characterized by a significant decrease in cortical acetylcholine that recovered to preanesthesia levels during recovery wakefulness. Corticocortical coherence and frontal–parietal symbolic transfer entropy in high γ band (85 to 155 Hz) were decreased during anesthetic-induced unconsciousness and returned to preanesthesia levels during recovery wakefulness. Sleep-wake states showed a state-dependent change in coherence and transfer entropy in high γ bandwidth, which correlated with behavioral arousal: high during wakefulness, low during SWS, and lowest during REM sleep. By contrast, frontal–parietal θ connectivity during sleep-wake states was not correlated with behavioral arousal but showed an association with well-established changes in cortical acetylcholine: high during wakefulness and REM sleep and low during SWS. Conclusions Corticocortical coherence and frontal–parietal connectivity in high γ bandwidth correlates with behavioral arousal and is not mediated by cholinergic mechanisms, while θ connectivity correlates with cortical acetylcholine levels.

Electroencephalogram Similarity Analysis Using Temporal and Spectral Dynamics Analysis for Propofol and Desflurane Induced Unconsciousness

“…These EEG dynamics similarities between them are in line with the findings that GABAergic neural circuit mechanisms behave [3,26,31]. This implies that highly structured thalamocortical oscillations that communicate with cortical information processing, as well as slow oscillations in cortical activity [9,32], which are responsible for this phenomenon.…”

“…This kind of anesthetic-induced and reversible unconsciousness state is known to be manipulated by anesthesiologists, bringing many benefits to humans, undoubtedly. Surprisingly, even with increasingly rich knowledge about anesthetic molecular pharmacology and clinical behavior, the underlying neural interaction circuit mechanisms for patient's consciousness is still far from being fully understood [3]. In practice, experienced anesthesiologists an induction agent for the sedation and maintenance one of general anesthesia.…”

Anesthesia with Dexmedetomidine and Low-dose Isoflurane Increases Solute Transport via the Glymphatic Pathway in Rat Brain When Compared with High-dose Isoflurane

“…The effect of norepinephrine blockade on the POA, in particular, has wide ranging ‘upstream’ effects involving several neurotransmitters and neural networks, leading to decreased arousal, sleep-like states or deep sedation 18 . In contrast, isoflurane (a halogenated inhalational anesthetic) exerts its effects by acting on a wide variety of voltage- and ligand-gated channels including GABA A , glycine, nicotinic acetylcholine receptors, NMDA and K channels 19,38 , which are located throughout the brain and spinal cord. The effects of isoflurane on LC neurons and NE are not as clear cut as those of dexmedetomidine.…”

Isoflurane Impairs Low-Frequency Feedback but Leaves High-Frequency Feedforward Connectivity Intact in the Fly Brain

“…Although a subset of studies show differing results (Barrett et al, 2012; Nicolaou et al, 2012; Maksimow et al, 2014), the disrupted frontal-parietal connectivity has also been demonstrated using functional magnetic resonance imaging (fMRI; Hudetz and Mashour, 2016). In addition, general anesthetic suppression of FB has also been reported in rodents (Imas et al, 2006; Pal et al, 2016), ferrets (Wollstadt et al, 2017), and monkeys (Lamme et al, 1998; Papadopoulou et al, 2015). Note, however, that Wollstadt et al (2017) show that FB (prefrontal cortex to V1) is reduced, but that this reduction may be a result of reduced “source information” within the prefrontal cortex.…”