Disruption of corticocortical information transfer during ketamine anesthesia in the primate brain

Schroeder, Karen E.; Irwin, Zachary T.; Gaidica, Matt; Bentley, J. Nicole; Patil, Parag G.; Mashour, George A.; Chestek, Cynthia A.

doi:10.1016/j.neuroimage.2016.04.039

Cited by 87 publications

(89 citation statements)

References 37 publications

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“…Ketamine appears to inhibit information transfer in cortical networks (Bonhomme et al, 2016; Schroeder et al, 2016), which may be a shared mechanism by which diverse anesthetics induce unconsciousness (Lee et al, 2013). Perturbations in cortical network connectivity also correlate with pathological brain states, such as depression (Muthukumaraswamy et al, 2015; Nugent et al, 2016), and ketamine-induced alterations in connectivity patterns may subserve its antidepressant effects (Muthukumaraswamy et al, 2015; Nugent et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

“…Ketamine has been found to functionally disrupt corticocortical connectivity with anesthetic dosing, and this pattern seems to follow a frontal-to-posterior direction (Figure 3; Lee et al, 2013; Blain-Moraes et al, 2014; Schroeder et al, 2016). This frontal-to-posterior disrupted cortical connectivity has been proposed as a mechanism of general anesthesia, having been demonstrated across a broad range of anesthetic drug classes during loss of consciousness (Lee et al, 2013).…”

Section: Proposed Mechanisms Of Actionsmentioning

confidence: 99%

“…Bonhomme et al (2016) presented functional MRI data from human volunteers whereby ketamine disrupted cortical connectivity between frontal and posterior cortices, while auditory and visual network integrity was maintained. A recent study used intracranial recordings to demonstrate direct, structural interruption of corticocortical sensory information transfer during ketamine-induced anesthesia in macaque monkeys (Schroeder et al, 2016). During anesthesia, somatosensory information transfer was maintained through thalamocortical pathways, though corticocortical information transfer was inhibited.…”

Section: Proposed Mechanisms Of Actionsmentioning

confidence: 99%

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Ketamine: 50 Years of Modulating the Mind

Vlisides

2016

Front. Hum. Neurosci.

252

204

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Ketamine was introduced into clinical practice in the 1960s and continues to be both clinically useful and scientifically fascinating. With considerably diverse molecular targets and neurophysiological properties, ketamine’s effects on the central nervous system remain incompletely understood. Investigators have leveraged the unique characteristics of ketamine to explore the invariant, fundamental mechanisms of anesthetic action. Emerging evidence indicates that ketamine-mediated anesthesia may occur via disruption of corticocortical information transfer in a frontal-to-parietal (“top down”) distribution. This proposed mechanism of general anesthesia has since been demonstrated with anesthetics in other pharmacological classes as well. Ketamine remains invaluable to the fields of anesthesiology and critical care medicine, in large part due to its ability to maintain cardiorespiratory stability while providing effective sedation and analgesia. Furthermore, there may be an emerging role for ketamine in treatment of refractory depression and Post-Traumatic Stress Disorder. In this article, we review the history of ketamine, its pharmacology, putative mechanisms of action and current clinical applications.

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Section: Discussionmentioning

confidence: 99%

Section: Proposed Mechanisms Of Actionsmentioning

confidence: 99%

Section: Proposed Mechanisms Of Actionsmentioning

confidence: 99%

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Ketamine: 50 Years of Modulating the Mind

Vlisides

2016

Front. Hum. Neurosci.

252

204

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“…Anesthetics with diverse molecular profiles and neurophysiological effects have been shown to fragment functional networks in the cortex, 1-5 and both sleep and anesthesia reduce surrogates of cortical information transfer. 4-12 Several recent studies encourage further investigation of the role of cortex in anesthetic-induced unconsciousness.…”

Section: Introductionmentioning

confidence: 99%

Neural Correlates of Wakefulness, Sleep, and General Anesthesia

et al. 2016

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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.

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“…1 Based on behavioral observations and the results of evoked potentials, Corssen and Domino also generated prescient insights regarding the state of brain networks during ketamine anesthesia. Recent neurophysiological data in human and nonhuman primates confirm that anesthetic doses of ketamine result in a unique constellation: 1) information can still be accurately represented in primary sensory cortex, 2 2) communication patterns between higher-order cortices become disrupted, 3 but 3) the complexity and repertoire of brain states are still consistent with disconnected consciousness (such as dreams or hallucinations). 4 Although there have been numerous studies of subanesthetic ketamine—as an analgesic, antidepressant, and psychotomimetic—using functional magnetic resonance imaging (fMRI), what has been notably absent is an fMRI investigation of brain networks during ketamine anesthesia.…”

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confidence: 99%