Abstract
Sevoflurane is widely used in adult and pediatric patients during clinical surgeries. Although studies have shown that exposure to sevoflurane impairs solfactory memory after an operation, the neuropathological changes underlying this effect are not clear. This study detected the effect of sevoflurane exposure on the development of calcium-binding proteins-expressing interneurons in the main olfactory bulb (MOB). We exposed neonatal mice to 2% sevoflurane at two different developmental time points and found that exposing mice to sevoflurane at postnatal day (PD) 7 significantly decreased the expression of GAD67 and parvalbumin (PV) in the olfactory bulb (OB) but did not alter the expression of calretinin (CR) or calbindin D28k (CB). The number and dendritic morphology of PV-expressing interneurons in the MOB were impaired by exposure to sevoflurane at PD7. However, exposure to sevoflurane at PD10 had no effect on calcium-binding protein expression or the number and dendritic morphology of PV-expressing interneurons in the MOB. These results suggest that exposing neonatal mice to sevoflurane during a critical period of olfactory development affects the development of PV-expressing interneurons in the MOB.
Highlights
Inhalation anesthetics are widely used in adult and pediatric patients during surgeries, and sevoflurane is one of the most frequently used inhalation anesthetics in infants and children because it has a low blood/gas ratio, low pungency and a rapid onset and recovery (Sakai et al, 2005; Edwards et al, 2010; Gibert et al, 2012)
We found that the laminar organization of the main olfactory bulb (MOB) was not adversely affected by sevoflurane exposure at either PD7 or PD10
Sevoflurane exposure at PD10 had no effect on calcium-binding protein-expressing interneurons in the MOB
Summary
Inhalation anesthetics are widely used in adult and pediatric patients during surgeries, and sevoflurane is one of the most frequently used inhalation anesthetics in infants and children because it has a low blood/gas ratio, low pungency and a rapid onset and recovery (Sakai et al, 2005; Edwards et al, 2010; Gibert et al, 2012). Animal studies have shown that exposing animals to inhalation anesthetics during critical developmental periods can induce neuropathologic changes and impair cognitive functions (Culley et al, 2003, 2004; Jevtovic-Todorovic et al, 2003; Fredriksson et al, 2007; Rammes et al, 2009). Exposing young rats to sevoflurane altered dendritic spine density during an important stage in synapse formation (Briner et al, 2010). These discoveries indicate that exposure to sevoflurane can affect the normal development of the brain. Studies have shown that inhaling anesthetic drugs can lead to olfactory dysfunction (Adelman, 1995; Fukumoto et al, 2005), there are few reports showing the neuropathologic changes in olfactory system induced by sevoflurane exposure
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