Spatial signatures of anesthesia-induced burst-suppression differ between primates and rodents

Abstract

During deep anesthesia, the electroencephalographic (EEG) signal of the brain alternates between bursts of activity and periods of relative silence (suppressions). The origin of burst-suppression and its distribution across the brain remain matters of debate. In this work, we used functional magnetic resonance imaging (fMRI) to map the brain areas involved in anesthesia-induced burst-suppression across four mammalian species: humans, long-tailed macaques, common marmosets, and rats. At first, we determined the fMRI signatures of burst-suppression in human EEG-fMRI data. Applying this method to animal fMRI datasets, we found distinct burst-suppression signatures in all species. The burst-suppression maps revealed a marked inter-species difference: in rats the entire neocortex engaged in burst-suppression, while in primates most sensory areas were excluded—predominantly the primary visual cortex. We anticipate that the identified species-specific fMRI signatures and whole-brain maps will guide future targeted studies investigating the cellular and molecular mechanisms of burst-suppression in unconscious states.

Disentangling the impact of cerebrospinal fluid formation and neuronal activity on solute clearance from the brain

“…We observed two different brain states, silent periods with burst-like phases during ISO anesthesia and enhanced neuronal activity with MED (Fig. 1E), in accordance with previous observations (31,32). The combination of both anesthetics revealed suppressed activity with burst-like phases comparable to the ISO anesthesia.…”

“…In our experiments, CSF formation was low with the carboanhydrase inhibitor AZE (48, 49), with no impact on neuronal activity. ISO modulates GABA A chloride channels and in our models was used to achieve low CSF formation together with low neuronal activity (31,32). Of the six anesthetic conditions used in our study, ISO + MED induced a condition, which most likely resembled sleep, characterized by high CSF formation and low neuronal activity.…”

“…Medetomidine (MED), an α 2 -adrenergic receptor agonist was used to achieve high CSF formation and high neuronal activity (1,(28)(29)(30). Iso urane (ISO) acting as a modulator of GABA A chloride channels was used to achieve lower CSF formation and reduced neuronal activity (31,32). The combination of both anesthetics was used to enhance CSF formation in a state of low neuronal activity.…”