Fading whispers down the lane: signal propagation in anaesthetized cortical networks

An active area of enquiry in the neuroscientific investigation of general anaesthesia is the question of whether anaesthetic-induced unconsciousness is mediated by bottom-up or top-down mechanisms in the brain. Candidates for the bottom-up approach include suppression of arousal centres in the brainstem and diencephalon,¹² activation of sleep-promoting neurones or nuclei in similar locations,¹³ blockade of sensory information en route from the thalamus to the cortex,⁴ and a disabled thalamic conductor for the neuronal orchestra of the cortex.⁵ Candidates for the top-down approach include direct effects on long-latency activity in cortical networks,⁶ with a consequent disruption of higher-order information synthesis that occurs beyond the level of the primary sensory cortex.^7–9 This bottom-up vs top-down distinction is almost surely artificial given the integrated circuits required for the normal function of neural systems and the widespread effects of general anaesthetics on the brain. We recently proposed that anaesthetics alter the level of consciousness (e.g. awake vs somnolent) through bottom-up mechanisms while degrading the contents of consciousness (e.g. the particular qualities of experience) through top-down mechanisms.¹⁰ Developing a clearer understanding of these processes is important because it can inform (i) the neurobiology of consciousness, a fundamental question in science, and (ii) our approach to brain monitoring, a fundamental and unmet challenge in clinical anaesthesia. However, it is difficult to address this question by investigating individual brain areas or molecular targets in the laboratory and also difficult to distinguish cortical and subcortical mechanisms through human neuroimaging and neurophysiology. In this issue of the British Journal of Anaesthesia, Hentschke and colleagues¹¹ examine an intermediate level of neuroanatomy and neurophysiology in a cortical slice model, finding more profound effects of isoflurane on signal propagation through the cortex than to the cortex.

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