Toward a Unified Theory of Narcosis: Brain Imaging Evidence for a Thalamocortical Switch as the Neurophysiologic Basis of Anesthetic-Induced Unconsciousness

Alkire, Michael T.; Haier, Richard J.; Fallon, James H.

doi:10.1006/ccog.1999.0423

Cited by 368 publications

(305 citation statements)

References 48 publications

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“…In addition, previous studies have suggested that the primary basis for anesthesia may be the blocking or disruption of sensory information processing through the thalamus (Angel, 1993), and assessment of regional uptake of glucose in deep anesthesia indicates that thalamus are more depressed (Alkire et al, 2000). But, in our study, it was very interesting that Fos was expressed in the PV, whereas there was no coexistence between Fos and GABA in this area because of the absence of GABAergic neurons.…”

Section: Discussioncontrasting

confidence: 43%

“…Studies from PET and electrophysiology indicated that in some brain regions, such as thalamus, hippocampus, inhalation anesthetic agents induced changes in glucose metabolic rate or postsynaptic potential (Gage and Robertson, 1985;Alkire et al, 2000), where anesthetic actions in these brain regions are known occur. However, there is still no morphological evidence about the functional targets of these inhalation anesthetic.…”

Section: Discussionmentioning

confidence: 99%

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The Effect of Sevoflurane Inhalation on Gabaergic Neurons Activation: Observation on the GAD67‐GFP Knock‐In Mouse

Han

Zhang

Wang

et al. 2010

The Anatomical Record

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The mechanisms underlying volatile anesthesia agents are not well elucidated. Emerging researches have focused on the participation of c-aminobutyric acid (GABA) neurons but there still lacks morphological evidence. To elucidate the possible activation of GABAergic neurons by sevoflurane inhalation in morphology, Fos (as neuronal activity marker) and GABA neurons double labeling were observed on the brain of glutamic acid decarboxylase (GAD) 67-GFP knock-in mice after sevoflurane inhalation. Twenty GAD67-GFP knock-in mice were divided into three groups: S1 group: incomplete anesthesia state induced by sevoflurane; S2 group: complete anesthesia state induced by sevoflurane; control(C) group. Sevoflurane induced a significant increase of Fos expression in the dorsomedial hypothalamic nucleus (DM), periaqueductal grey (PAG), hippocampus (CA1, DG), paraventricular thalamic nucleus (PV), lateral septal nucleus (LS), and cingulate cortex (Cg1 and Cg2) in S1 group compared to C group, and increase of Fos expression in S2 group compared to S1 group. In S2 group, Fos was only expressed in the medial amygdaloid nucleus (MeA), Edinger-Westphal (E-W) nucleus, arcuate hypothalamic nucleus (Arc) and the ventral part of paraventricular hypothalamic nucleus (PaV). Double immunofluroscent staining indicated that in LS, almost all Fos were present in GABAergic neurons. In CA1, DG, DM, cg1, cg2, and PAG, Fos was expressed as well, but only few were present in GABAergic neurons. Fos expression was very high in thalamus, but no coexistence were found as no GABAergic neuron was detected in this area. Our results provided morphological evidence that GABAergic transmission in specific brain areas may participate in the sevoflurane-induced anesthesia. Anat Rec, 293:2114Rec, 293: -2122

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Section: Discussioncontrasting

confidence: 43%

Section: Discussionmentioning

confidence: 99%

The Effect of Sevoflurane Inhalation on Gabaergic Neurons Activation: Observation on the GAD67‐GFP Knock‐In Mouse

Han

Zhang

Wang

et al. 2010

The Anatomical Record

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“…The chemical diversity of anesthetic compounds suggests that a diversity of brain structures are affected. Recent attempts with fMRI, PET, and quantitative EEG studies on anesthesia in human brains support this suspicion, and allow us to construct tentatively a minimal model of what structures are critically involved in anesthesia (Alkire et al, 2000;Cariani, 2000;John, 2001). Figure 1 illustrates schematically this minimal model, mainly taken from Alkire et al (2000).…”

Section: Macroscopic Effectsfmodification Of Thalamocortical Loop Actmentioning

confidence: 92%

“…Recent attempts with fMRI, PET, and quantitative EEG studies on anesthesia in human brains support this suspicion, and allow us to construct tentatively a minimal model of what structures are critically involved in anesthesia (Alkire et al, 2000;Cariani, 2000;John, 2001). Figure 1 illustrates schematically this minimal model, mainly taken from Alkire et al (2000). The key components form a triangular network of corticothalamic, thalamocortical, and reticulothalamic neurons, comprising both positive and negative feedback loops.…”

Section: Macroscopic Effectsfmodification Of Thalamocortical Loop Actmentioning

confidence: 95%

“…Different forms of oscillatory activity are associated with different functional states; generally, and rather vaguely, high-frequency activity, in single neurons reflected as tonic firing, has been associated with conscious states, while low-frequency activity, and single neuron burst firing, have been said to characterize unconscious states (see Alkire et al, 2000). How do general anesthetics induce the required shifts of activity?…”

Section: Mesoscopic Effectsfdisrupted Coherence?mentioning

confidence: 99%

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Mechanisms of Anesthesia: Towards Integrating Network, Cellular, and Molecular Level Modeling

Århem

Klement

Nilsson

2003

Neuropsychopharmacol

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The mechanisms of anesthesia are surprisingly little understood. The present article summarizes current knowledge about the function of general anesthetics at different organization levels of the nervous system. It argues that a consensus view can be constructed, assuming that general anesthetics modulate the activity of ion channels, the main targets being GABA and NMDA channels and possibly voltagegated and background channels, thereby hyperpolarizing neurons in thalamocortical loops, which lead to disruption of coherent oscillatory activity in the cortex. Two computational cases are used to illustrate the possible importance of molecular level effects on cellular level activity. Subtle differences in the mechanism of ion channel block can be shown to cause considerable differences in the modification of the oscillatory activity in a single neuron, and consequently in an associated network. Finally, the relation between the anesthesia problem and the classical consciousness problem is discussed, and some consequences of introducing the phenomenon of degeneracy into the picture are pointed out.

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Neural Correlates of Consciousness as State and Trait

Stoerig

2006

Encyclopedia of Cognitive Science

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Toward a Unified Theory of Narcosis: Brain Imaging Evidence for a Thalamocortical Switch as the Neurophysiologic Basis of Anesthetic-Induced Unconsciousness

Cited by 368 publications

References 48 publications

The Effect of Sevoflurane Inhalation on Gabaergic Neurons Activation: Observation on the GAD67‐GFP Knock‐In Mouse

The Effect of Sevoflurane Inhalation on Gabaergic Neurons Activation: Observation on the GAD67‐GFP Knock‐In Mouse

Mechanisms of Anesthesia: Towards Integrating Network, Cellular, and Molecular Level Modeling

Neural Correlates of Consciousness as State and Trait

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