Aims: The aim of this study was to investigate the role of depolarizing activation of Na-Ca exchanger (NCX) by oligodendrocyte progenitor cells (OPC) in the effect of sevoflurane on myelination.
Main Methods: On postnatal days 7, 8, and 9, mice were exposed to 3 % sevoflurane for 2 h per day. The proliferation, differentiation, and myelin sheath of OPC were observed with immunofluorescence, quantitative real-time polymerase chain reaction (QRT-PCR), and transmission electron microscopy (TEM) at various time points. The open field, Y maze, and new object recognition tests were used to measure spatial learning and memory. siRNA was used for the knockdown NCX1 in human OPC (HOPC) before sevoflurane exposure; the Transwell migration assay was used to measure cell migration ability and Fluo 4-AM was used to measure intracellular Ca2+ concentration.
Key Findings: Pretreatment with an NCX inhibitor attenuated the proliferation and differentiation of OPC induced by sevoflurane and induced a remarkable increase in platelet-derived growth factor receptor-alpha (PDGFRα), 2, 3-cyclic nucleotide 3-phosphodiesterase (CNPase), oligodendrocyte transcription factor 2 (Olig2), and homeodomain protein NK2 homeobox 2 (NKX2.2) levels. Pretreatment with an NCX inhibitor alleviated the sevoflurane-induced myelination disorder and cognitive impairment. The decreased cell migration and increased intracellular Ca concentration observed in the siRNA-negative control group was reversed in the sevoflurane plus siRNA-NCX1 group.
Significance: This study suggests that repeated sevoflurane exposure in newborn mice leads to depolarization of OPC, which leads to Ca influx through NCX and affects OPC proliferation, migration, differentiation, and myelination, ultimately leading to cognitive impairment.
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| http://dx.doi.org/10.1016/j.lfs.2022.120951 | DOI Listing |
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