Recent population studies suggest that children who receive anesthesia and surgery could be at an
increased risk for developing learning disabilities. The underlying reason for this clinical observation is largely
unknown. Whether undergoing anesthesia contributes to learning disability development, or if the need for
anesthesia and surgery is a marker for other unidentified factors that contribute to the development of learning
disabilities, remains to be determined. Neurogenesis, regulated by the Wnt-catenin signaling pathway, has
been shown to be involved in learning and memory, and sevoflurane is the most commonly used inhalation
anesthetic in children. We therefore set out to determine the effects of sevoflurane on neurogenesis and the
Wnt-catenin signaling pathway in mouse neural progenitor cells (NPCs) using immunofluorescence and
Western blot analysis. Here we show for the first time that 4.1%, but not 2.0%, sevoflurane reduced mouse
NPC proliferation, increased Glycogen synthase kinase-3β(GSK-3β) levels, and decreased levels of β-Catenin
in mouse NPCs. The GSK-3β inhibitor Lithium attenuated the sevoflurane-induced reduction in mouse NPC
proliferation. The data suggest that sevoflurane may reduce neurogenesis through the Wnt-catenin signaling
pathway. These findings would promote further studies to investigate the effects of anesthesia on
neurogenesis and function of learning and memory, as well as the underlying mechanisms in vitro and in vivo.
Ultimately these efforts would lead to safer anesthesia care and better postoperative outcomes in children.