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Hypoxic-ischemic (HI) brain injury in the perinatal period is one of the most important factors of neonatal mortality and subsequent sequelae.The combined effects of cellular energy failure, acidosis, glutamate release, intracellular Ca2+ accumulation, lipid peroxidation, and nitric-oxide neurotoxicity can lead to neuronal apoptosis and necrosis, and then result in the loss of neurons.At the same time, the changes of neural functions should be earlier than the morphological changes; well there is still no report about these.In this study, animals were divided into control group and hypoxia-ischemia group.The HI brain injury rat model was obtained by unilateral occlusion of left carotid artery, followed by exposure to hypoxia (92% N2, 8% O2) for 1.5 h at 7-day-old rats.The patch clamp, immunohistochemistry and western bloting technologies were used to test the normal electrophysiological properties, the excitatory postsynaptic currents (EPSCs), the expression and disposition of synaptophysin, VGluT1, NMDAR, and AMPAR of hippocampal CA1 area pyramidal cells immediately after HI injury and control.Compared with the naive control group, CA1 pyramidal neurons of HI models showed that the excitabilities of HI injury hippocampal CA1 pyramidal cells were decreased and the amplitude and duration of EPSCs were increased.The expression of synaptophysin, NMDAR, and AMPAR was not changed, while the expression of VGluT1 was lower than the control group.All of these results indicated that the decrease of neural excitability of HI injury models was the protective responses of neurons, but the damage of HI brain injury was beyond the ability of self-protection.Therefore, giving the proper treatment after injury was very necessary.