ABSTRACT
Objective To evaluate the role and mechanism of ifenprodil, which is the selective antagonist of N-methyl-D-aspartic acid subtype receptor NR2B, in soflurane-induced cognitive dysfunction in neonatal rats.Methods Twenty-eight 7-day-old Sprague Dawley rats, weighing 15-18 g, were randomly divided into 4 groups (n=7 each): control group (group C), ifenprodil group (group I), sevoflurane group (group S) and ifenprodil+sevoflurane group (group IS).Normal saline 0.2 ml was injected intraperitoneally in group C.Specific NR2B receptor antagonist ifenprodil 5 mg/kg was injected intraperitoneally at the corresponding time points in group I.Normal saline 0.2 ml was injected intraperitoneally and 2.0% sevoflurane was inhaled for 4 h in group S.Ifenprodil 5 mg/kg was injected intraperitoneally 2 h before sevoflurance inhalation, and 2.0% sevoflurance was inhaled for 4 h in group IS.The rats were then sacrificed 3 weeks after administration, their brains were immediately removed and hippocampal slices were prepared for electrophyisological experiments.The value of population spike amplitude (PSA) and long-term potentiation (LTP) were measured every 10 minutes.Induced LTP was recorded.Results Compared with group C, the values of PSA and rates of induced LTP were significantly decreased in group S (P＜0.01).The values of PSA and rates of induced LTP were significantly increased in group IS than those in group S (P＜0.01).Conclusion NR2B receptor is involved in sevoflurance-induced cognitive dysfunction in the neonatal rats.Pretreatment with ifenprodil 5.0 mg/kg can improve the neurotoxicity and protect the brain.