The effect of sevoflurane and isoflurane anesthesia on single unit and local field potentials
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Volatile general anesthetics are used commonly in adults and children, yet their mechanisms of action are complex and the changes in single unit firing and synaptic activity that underlie the broad decreases in neuronal activity induced by these drugs have not been well characterized. Capturing such changes throughout the anesthesia process is important for comparing the effects of different anesthetics and gaining a better understanding of their mechanisms of action and their impact on different brain regions. Using chronically implanted electrodes in the rabbit somatosensory cortex, we compared the effects of two common general anesthetics, isoflurane, and sevoflurane, on cortical neurons. Single unit activity and local field potentials (LFP) were recorded continuously before and during anesthetic delivery at 1 MAC, as well as during recovery. Our findings show that although isoflurane and sevoflurane belong to the same class of volatile general anesthetics, their effects upon cortical single units and LFP were quite different. Overall, the suppression of neuronal firing was greater and more uniform under sevoflurane. Moreover, the changes in LFP frequency bands suggest that effect of anesthesia upon beta oscillations does not necessarily depend on the level of single unit activity, but rather on the changes in GABA/glutamate neurotransmission induced by each drug.
KeywordsLocal field potentials Beta oscillations Volatile anesthetics Single-neuron activity
This work was supported by the National Institute of General Medical Sciences (R01GM112715).
Compliance with ethical standards
Conflict of interest
All authors declared no conflict of interest.
- Anderson PM, Jones NC, O’Brien TJ, Pinault D (2017) The N-methyl d-aspartate glutamate receptor antagonist ketamine disrupts the functional state of the corticothalamic pathway. Cereb Cortex 27:3172–3185Google Scholar
- Prabhakar NR, Semenza GL (2015) Oxygen sensing and homeostasis. Physiology (Bethesda) 30:340–348Google Scholar