Authors: Jinyang Liu, M.S. et al
Anesthesiology 3 2018, Vol.128, 555-563.
Background: This study tests the hypothesis that sevoflurane blocks long-term potentiation only if it is present during the high-frequency stimulation that induces long-term potentiation.
Methods: Long-term potentiation, an electrophysiologic correlate of memory, was induced by high-frequency stimulation and measured as a persistent increase in the field excitatory postsynaptic potential slope in the CA1 region.
Results: Long-term potentiation was induced in the no sevoflurane group (171 ± 58% vs. 96 ± 11%; n = 13, mean ± SD); when sevoflurane (4%) was present during the high-frequency stimulation, long-term potentiation was blocked (92 ± 22% vs. 99 ± 7%, n = 6). While sevoflurane reduced the size of the field excitatory postsynaptic potential to single test stimuli by 59 ± 17%, it did not significantly reduce the size of the field excitatory postsynaptic potentials during the 100 Hz high-frequency stimulation. If sevoflurane was removed from the artificial cerebrospinal fluid superfusing the slices 10 min before the high-frequency stimulation, then long-term potentiation was induced (185 ± 48%, n = 7); this was not different from long-term potentiation in the no sevoflurane slices (171 ± 58). Sevoflurane before, but not during, ⊖-burst stimulation, a physiologic stimulus, did not block the induction of long-term potentiation (151 ± 37% vs. 161 ± 34%, n = 7).
Conclusions: Sevoflurane blocks long-term potentiation formation if present during the high-frequency stimulation; this blockage of long-term potentiation does not persist if sevoflurane is discontinued before the high-frequency stimulation. These results may explain why short periods of insufficient sevoflurane anesthesia may lead to recall of painful or traumatic events during surgery.
What We Already Know about This Topic
- Sevoflurane administration, in appropriate doses, produces amnesia in part by facilitating γ-aminobutyric acid–mediated inhibition and decreasing N-methyl-D-aspartate–mediated excitation. These effects are rapidly reversed upon cessation of sevoflurane administration.
- Sevoflurane also triggers changes in signal transduction systems, some of which play a central role in memory formation that persist for some time. Whether these changes in signal transduction impact memory function after discontinuation of sevoflurane is not clear.
What This Article Tells Us That Is New
- Sevoflurane administration during the stimulation that induces long-term potentiation also reduced long-term potentiation, a model for memory formation, in the hippocampus. Long-term potentiation was not blocked if sevoflurane was discontinued before the stimulus that induces long-term potentiation.
- The results suggest that sevoflurane can suppress memory formation only during its administration. The persistent effects on signal transduction do not prevent the recovery of memory formation.