General anaesthesia: from molecular targets to neuronal pathways of sleep and arousal
By Nicholas P. Franks. Nature Reviews Neuroscience, 2008
1,272 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience
View Paper: https://www.semanticscholar.org/paper/1eac826c2119cfec978927f6e8bfe1e30e008e2d
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cellular and Molecular Neuroscience
- Jean-Pierre Changeux
- Marcello Massimini
- Stanislas Dehaene
- Melanie Boly
- Pierre Boveroux
- István Módy
- Steven Laureys
- Michael D. Greicius
In Cognitive Neuroscience
- Stanislas Dehaene
- Jean-Pierre Changeux
- Melanie Boly
- Audrey Vanhaudenhuyse
- Marie-Aurélie Bruno
- Marcello Massimini
- Steven Laureys
- Christophe L. M. Phillips
Citations in the corpus
- The spectral exponent of the resting EEG indexes the presence of consciousness during unresponsiveness induced by propofol, xenon, and ketamine (2019, positive): “Besides its antagonizing action on NMDA receptors, xenon acts primarily on two-pore-domain Kþ (2 PKþ) channels, strongly potentiating 2 PKþ conductance (Franks, 2008).”
- Extrasynaptic GABAA receptors: Their function in the CNS and implications for disease (2012, background): “Drugs that modulate sleep and induce anesthesia share common molecular targets (Franks, 2008).”
- Breakdown of within- and between-network Resting State Functional Magnetic Resonance Imaging Connectivity during Propofol-induced Loss of Consciousness (2010, background): “Brainstem sleep-promoting neurons have also been shown to be potentially involved in the mechanisms of anesthesia-induced unconsciousness.(7) Recent evidence suggests that cortical activity better correlates with propofol-induced sedative effects than (sub)thalamic activity.”
- Experimental and theoretical approaches to conscious processing. (2011, background): “Anesthetic-induced loss of consciousness usually coincides with the disruption of activity in extensive regions of cerebral cortex, particularly the precuneus, posterior cingulate cortex, cuneus, localized regions of the lateral frontal and parietal cortices, and occasionally the cerebellum (Franks,”