Does Memory Consolidation by Anesthetics Relate to a Time Window of Age?

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Zhou et al1 have demonstrated that exposure to 1.5% isoflurane for 1 hour prevented the depression of long-term potentiation caused by the β-amyloid peptide Aβ1–42 in the hippocampal slices from 3- to 4-week-old rats. Aβ1–42 is the predominant form of β-amyloid peptide in neuronal plaques, which are robustly associated with the pathogenesis of Alzheimer disease, indicating that the isoflurane clinical dose alleviates the derangement of long-term memory consolidation induced by neurotoxic substances.2 I read the article with interest because the rodents that Zhou et al1 used are compatible with humans of 4 to <10 years of age.3 We also recently have documented that 2.5% sevoflurane exposure for 3 hours to 4-week-old mice accelerates the long-term memory.4 The increase in cytoskeletal protein F-actin constitution with the small GTPase rac1 overexpression in the hippocampus coexisted with the phenomenon, strongly suggesting the enhancement of synaptic plasticity.4 Therefore, the inhalation of volatile anesthetics within clinical doses may amplify long-term memory consolidation in a particular time window of ages such as immediately before and early adolescence.
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