新生大鼠缺氧缺血后远期海马CA_1区神经元和突触的变化及药物干预的效果

Changes of Pyramidal Neurons and Synapses in the Hippocampal CA 1 Region in Brains of Neonatal Rats after Hypoxia ischemia and Drug Intervention

目的 了解缺氧缺血对新生大鼠脑神经元和突触的影响及１６ 二磷酸果糖（ＦＤＰ）、硫酸镁（ＭｇＳＯ４）、苯巴比妥（ＰＢ）三种药物急性期干预治疗的作用，评价早期治疗的远期疗效。 方法 ７ 日龄Ｗｉｓｔａｒ 大鼠行左侧颈总动脉结扎，吸入８ ％ 氧气２ 小时，立即腹腔注射ＦＤＰ、ＭｇＳＯ４ 、ＰＢ５日，于生后２８ 天断头、取左侧脑海马，用Ｄｉｓｅｃｔｏｒ 方法计数海马ＣＡ１ 区锥体神经元；用体视学方法及计算机图象分析仪测量、计算突触数密度、圆盘面积和表面密度。 结果 缺氧缺血使新生大鼠脑神经元和突触的数密度减小，突触表面密度减小，而突触大小无变化，神经元减少更明显。三种药物均可使脑神经元和突触的数密度增大，突触表面密度增大。 结论 缺氧缺血影响了新生大鼠脑的发育，三种药物急性期干预治疗对脑发育均有改善作用。

Objective To study the long term effect of perinatal hypoxic brain damage on neurons and synapses,and to find an effective approach of drug intervention. Methods We set up an animal model of hypoxia ischemia using 7 day old Wistar rats and observed morphological changes of pyramidal neurons and synapses in the hippocampal CA 1 region 21 days after hypoxia ischemia in vivo (28 days after birth).We also observed the protective effect of FDP(froctose 1 6 diphosphate),MgSO 4(magnesium sulfate) and PB (phenobarbital) during the acute phase of hypoxia ischemia on future neurons and synapses. Results The numerical density of pyramidal neurons and synapses in the hippocampal CA 1 region decreased 21 days after hypoxia ischemia,surface density of synapses also decreased,though the average area of single synaptic junction was unchanged.Decrease of neurons in number is more evident than that of synapses.Acute phase intervention with FDP,MgSO 4 and PB helped to prevent pyramidal neurons death,to increase the numerical and surface density of synapses. Conclusion Brain development of rats in our model was hampered in pyramidal neurons and synapses.Intervention with FDP,MgSO 4 and PB during acute phase can help to reduce damage to future brain development.