• Woosuk Chung, Min Jeong Ryu, Jun Young Heo, Soomin Lee, Seunghwan Yoon, Haram Park, Sangil Park, Yangsik Kim, Yoon Hee Kim, Seok Hwa Yoon, Yong Sup Shin, Won Hyung Lee, Xianshu Ju, Gi Ryang Kweon, and Youngkwon Ko.
• From the Department of Anesthesia and Pain Medicine, Chungnam National University, Daejeon, South Korea (W.C., S.L., S.Y., S.P., Y.H.K., S.H.Y., Y.S.S., W.H.L., Y.K.); Departments of Biochemistry (M.J.R., J.Y.H., G.R.K.) and Medical Science (J.Y.H., X.J.), Chungnam National University School of Medicine, Daejeon, South Korea; and Departments of Biological Sciences (H.P.) and Biomedical Sciences (Y.K.), Korea Advanced Institute of Science and Technology, Daejeon, South Korea.
• Anesthesiology. 2017 Feb 1; 126 (2): 288-299.

BackgroundAnesthesia during the synaptogenic period induces dendritic spine formation, which may affect neurodevelopment. The authors, therefore, evaluated whether changes in synaptic transmission after dendritic spine formation induced by sevoflurane were associated with long-term behavioral changes. The effects of sevoflurane on mitochondrial function were also assessed to further understand the mechanism behind spinogenesis.MethodsPostnatal day 16 to 17 mice were exposed to sevoflurane (2.5% for 2 h), and synaptic transmission was measured in the medial prefrontal cortex 6 h or 5 days later. The expression of postsynaptic proteins and mitochondrial function were measured after anesthesia. Long-term behavioral changes were assessed in adult mice.ResultsSevoflurane increased the expression of excitatory postsynaptic proteins in male and female mice (n = 3 to 5 per group). Sevoflurane exposure in male mice transiently increased miniature excitatory postsynaptic current frequency (control: 8.53 ± 2.87; sevoflurane: 11.09 ± 2.58) but decreased miniature inhibitory postsynaptic current frequency (control: 10.18 ± 4.66; sevoflurane: 6.88 ± 2.15). Unexpectedly, sevoflurane increased miniature inhibitory postsynaptic current frequency (control: 1.81 ± 1.11; sevoflurane: 3.56 ± 1.74) in female mice (neurons, n = 10 to 21 per group). Sevoflurane also increased mitochondrial respiration in male mice (n = 5 to 8 per group). However, such changes from anesthesia during the critical period did not induce long-term behavioral consequences. Values are presented as mean ± SD.ConclusionsSevoflurane exposure during the critical period induces mitochondrial hyperactivity and transient imbalance of excitatory/inhibitory synaptic transmission, without long-lasting behavioral consequences. Further studies are needed to confirm sexual differences and to define the role of mitochondrial activity during anesthesia-induced spine formation.

28 keywords...

hide…