Abstract
Objective To evaluate the role of gamma-aminobutyric acid A (GABAA) receptor in isoflurane-induced cognitive dysfunction in neonatal rats.Methods Twenty-eight 7-day-old Sprague Dawley rats,weighing 16-18 g,were randomly divided into 4 groups (n =7 each):control group (group Con),securinine group (group See),isoflurane group (group Iso) and securinine + isoflurane group (group Sec + Iso).Normal saline 0.2 ml was injected intraperitoneally in group Con.Specific GABAA receptor antagonist securinine 30 mg/kg was injected intraperitoneally at the corresponding time points in group Sec.Normal saline 0.2 ml was injected intraperitoneally and 1.4% isoflurane was inhaled for 6 h in group Iso.Securinine 30 mg/kg was injected intraperitoneally at 30 min before isoflurane inhalation and 3 h of inhalation,and 1.4% isoflurane was inhaled for 6 h in group Sec + Iso.The rats were then sacrificed at 3 weeks after administration,their brains were immediately removed and hippocampal slices were prepared for electrophysiological experiments.The value of population spike amplitude (PSA) and long-term potentiation (LTP) were measured every 5 min.The successful LTP induction was recorded.Results Compared with group Con,the values of PSA and rates of successful LTP induction were significantly decreased in group Iso (P < 0.01),and no significant change was found in the parameters mentioned above in groups Sec and Sec + Iso (P > 0.05).The values of PSA and rates of successful LTP induction were significantly higher in group Sec + Iso than in group Iso (P < 0.01).Conclusion GABAA receptor is involved in isoflurane-induced cognitive dysfunction in the neonatal rats. Key words: Receptors, GABA; Isoflurane; Cognition disorders; Infant, newborn
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