Lesion of cholinergic neurons in nucleus basalis enhances response to general anesthetics

Leung, L. Stan; Petropoulos, Sophie; Shen, Bixia; Luo, Tao; Herrick, Ian A.; Rajakumar, Nagalingam; Ma, Jingyi

doi:10.1016/j.expneurol.2011.01.019

Cited by 32 publications

(25 citation statements)

References 58 publications

(84 reference statements)

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“…This finding may suggest a partial dissociation between immobility and loss of consciousness whereby SS animals were unconscious but not incapable of responding due to an anesthetic suppression of motor responses at M1. 24 Furthermore, complete correlation between electroencephalogram responses and behavioral responses in the anesthetized setting may not be a valid expectation because motor (behavioral) responses involve many steps, including spinal cord transmission, peripheral neuronal function and muscle response.…”

Section: Discussionmentioning

confidence: 99%

Strain Differences in Cortical Electroencephalogram Associated with Isoflurane-induced Loss of Consciousness

et al. 2013

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Introduction Previously observed increased sensitivity to noxious stimulation in the Dahl salt-sensitive rat strain (SS/JrHsdMcwi, abbreviated as SS) compared to Brown Norway rats (BN/NhsdMcwi abbreviated as BN) is mediated by gene(s) on a single chromosome. The present study used behavioral and electrocortical data to determine if differences also exist between SS and BN in loss of consciousness. Methods Behavioral responses, including loss of righting, (a putative index of consciousness) and concurrent electroencephalogram recordings, in twelve SS and BN rats were measured during isoflurane at inhaled concentrations of 0, 0.3, 0.6, 0.8, 1.0 and 1.2%. Results In SS compared to BN, the mean ± SEM EC50 for righting was significantly less (0.65 ± 0.01% vs 0.74 ± 0.02% inhaled isoflurane) and delta fraction in parietal electroencephalogram was enhanced 50 - 100% at all isoflurane levels during emergence. The frequency decay constant of the exponential fit of parietal electroencephalogram spectrum graphed as a function of isoflurane level was 3 times less steep (mean ± SEM slope −57 ± 13 vs −191 ± 38) and lower at each level of isoflurane in SS vs BN (i.e. shifted toward low frequency activity). Electroencephalogram differences between strains were larger during emergence than induction. Conclusions Sensitivity is higher in SS compared to BN leading to unconsciousness at lower levels of isoflurane. This supports using additional strains in this animal model to study the genetic basis for differences in anesthetic action on mechanisms of consciousness. Moreover, induction and emergence appear to involve distinct pathways.

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Section: Discussionmentioning

confidence: 99%

Strain Differences in Cortical Electroencephalogram Associated with Isoflurane-induced Loss of Consciousness

et al. 2013

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“…These observations suggest that the absence of basal forebrain cholinergic neurons promotes cortical synchronization and increased sensitivity to anesthetics. However, loss of these cholinergic neurons did not alter the duration of the response to tail pinch or righting after halothane [74]. These results implicate the cholinergic neurons of the basal forebrain in mediating sensitivity to propofol or pentobarbital, but not halothane.…”

Section: Basal Forebrainmentioning

confidence: 99%

Sleep and Anesthesia Interactions: A Pharmacological Appraisal

Scharf

Kelz

2012

Curr Anesthesiol Rep

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Anesthetics have been used in clinical practice for over a hundred years, yet their mechanisms of action remain poorly understood. One tempting hypothesis to explain their hypnotic properties posits that anesthetics exert a component of their effects by “hijacking” the endogenous arousal circuitry of the brain. Modulation of activity within sleep- and wake-related neuroanatomic systems could thus explain some of the varied effects produced by anesthetics. There has been a recent explosion of research into the neuroanatomic substrates affected by various anesthetics. In this review, we will highlight the relevant sleep architecture and systems and focus on studies over the past few years that implicate these sleep-related structures as targets of anesthetics. These studies highlight a promising area of investigation regarding the mechanisms of action of anesthetics and provide an important model for future study.

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“…Some of the primarily affected neurotransmitter receptors were tested experimentally for a causal role in the components of anesthesia (Alkire et al. 2007; Leung et al. 2011).…”

Section: Levels Of Understanding Anesthesiamentioning

confidence: 99%

“…1999; Perry and Perry 2004). In particular, a reduction in ACh activity in the ascending projections from nucleus basalis to the cortex may contribute to immobility (Leung et al. 2011).…”

Section: Are There Group Specific Neurochemical Effects Of General Anmentioning

confidence: 99%

The in vivo neurochemistry of the brain during general anesthesia

Müller

Pum²,

Amato

et al. 2011

Journal of Neurochemistry

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J. Neurochem. (2011) 119, 419–446. Abstract Anesthesia describes a complex state composed of immobility, amnesia, hypnosis (sleep or loss of consciousness), analgesia, and muscle relaxation. Bottom‐up approaches explain anesthesia by an interaction of the anesthetic with receptor proteins in the brain, whereas top‐down approaches consider predominantly cortical and thalamic network activity and connectivity. Both approaches have a number of explanatory gaps and as yet no unifying view has emerged. In addition to a direct interaction with primary target receptor proteins, general anesthetics have massive effects on neurotransmitter activity in the brain. They can change basal transmitter levels by interacting with neuronal activity, transmitter synthesis, release, reuptake and metabolism. By that way, they can affect a great number of neurotransmitter systems and receptors. Here, we review how different general anesthetics affect extracellular activity of neurotransmitters in the brain during induction, maintenance, and emergence from anesthesia and which functional consequences this may have. Commonalities and differences between different groups of anesthetics in their action on neurotransmitter activity are discussed. We also review how general anesthetics affect the response dynamics of the neurotransmitter systems after sensory stimulation. More than 30 years of research have now yielded a complex picture of the effects of general anesthetics on brain neurotransmitter basal activity and response dynamics. It is suggested that analyzing the effects on neurotransmitter activity is the logical next step after protein interactions in a bottom‐up analysis of anesthetic action in the brain on the way to a unifying view of anesthesia.

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Lesion of cholinergic neurons in nucleus basalis enhances response to general anesthetics

Cited by 32 publications

References 58 publications

Strain Differences in Cortical Electroencephalogram Associated with Isoflurane-induced Loss of Consciousness

Strain Differences in Cortical Electroencephalogram Associated with Isoflurane-induced Loss of Consciousness

Sleep and Anesthesia Interactions: A Pharmacological Appraisal

The in vivo neurochemistry of the brain during general anesthesia

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