Abstract

Objective To discuss the effects of hippocampal Na+-K+ -2C1- cotransporter (NKCC1) on sevoflurane-induced neurobehavioral impairments in neonatal rats. Methods Thirty six 6-day-old male Sprague-Dawley rats were divided into three groups (n=12), according to the random number table method: a control group (group C), a sevoflurane group (group S), and a sevoflurane + bumetanide group (group SB). Group C inhaled 30% oxygen for 6 h, while groups S and SB inhaled 2.1% sevoflurane+30% oxygen for 6 h. Group SB was intraperitoneally injected with bumetanide (1.82 mg/kg) 15 min before sevoflurane inhalation. Then, 4 weeks later, the elevated plus maze and prepulse inhibition (PPI) tests were performed. One week after behavior tests, the hippocampus was harvested. Quantitative real time PCR and Western blot were used to detect the levels of NKCC1 mRNA and protein. Results In the elevated plus maze test, no significant difference was observed in total movement distance among the three groups (P<0.05). Compared with group C, group S spent shortened time of stay in the open arms, presented decreased PPI% corresponding to PP3 and PP6 (P<0.05), and produced increased amounts of hippocampal NKCC1 mRNA and protein (P<0.05). Compared with group S, group SB presented extended time in the open arms, increased PPI% corresponding to PP3 and PP6, and declined amounts of hippocampal NKCC1 mRNA and protein (P<0.05). Conclusions Sevoflurane may cause neurobehavioral damages in neonatal rats, which may be associated with NKCC1. Key words: Sevoflurane; Na+-K+ -2C1- cotransporter; Hippocampus; Neuroethology; Neonatal rats

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