Objective To explore the changes in spatial learning performance and long-term potentiation(LTP)which is recognized as a component of the cellular basis of learning and memory in normal and lead-exposed rats after adm...Objective To explore the changes in spatial learning performance and long-term potentiation(LTP)which is recognized as a component of the cellular basis of learning and memory in normal and lead-exposed rats after administration of melatonin (MT)for two months.Methods Experiment was performed in adult male Wistar rats(12 controls,12 exposed to melatonin treatment,10 exposed to lead and 10 exposed to lead and melatonin treatment).The lead-exposed rats received 0.2%lead acetate solution from their birth day while the control rats drank tap water.Melatonin(3 mg/kg)or vehicle was administered to the control and lead-exposed rats from the time of their weaning by gastric gavage each day for 60 days,depending on their groups.At the age of 81-90 days.all the animals were subjected to Morris water maze test and then used for extracellular recording of LTP in the dentate gyrus(DG)area of the hippocampus in vivo.Results Low dose of melatonin given from weaning for two months impaired LTP in the DG area of hippocampus and induced learning and memory deficit in the control rats.When melatonin was administered over a prolonged period to the lead-exposed rats,it exacerbated LTP impairment.learning and memory deficit induced by lead.Conclusion Melatonin is not suitable for normal and lead-exposed children.展开更多
目的:探讨海马内注射β-amyloid protein 25-35(Aβ25-35)所致Alzheizer’s病(AD)模型大鼠空间学习记忆功能障碍的海马突触可塑性长时程增强(LTP)机制,为联合开展AD动物行为学和在体电生理学研究提供实验证据。方法:在脑立体定位仪上给...目的:探讨海马内注射β-amyloid protein 25-35(Aβ25-35)所致Alzheizer’s病(AD)模型大鼠空间学习记忆功能障碍的海马突触可塑性长时程增强(LTP)机制,为联合开展AD动物行为学和在体电生理学研究提供实验证据。方法:在脑立体定位仪上给予大鼠双侧海马分别注射4 nmol/L Aβ25-35或等体积生理盐水每侧2μl,手术后恢复2周,每只大鼠依次进行行为学和电生理两部分实验。首先,利用Morris水迷宫进行空间学习、记忆功能测试;之后,进行在体海马CA1区场兴奋性突触后电位(fEPSP)引导记录实验,观察突触可塑性指标长时程增强(LTP)的改变。结果:与对照组相比,海马内注射Aβ25-35大鼠的空间学习记忆功能和在体海马突触可塑性LTP均有改变,其中:逃避潜伏期和逃避距离明显增加(P<0.01);目标象限内游泳时间和距离明显缩短(P<0.01);在体海马LTP幅度显著降低(P<0.01)。结论:海马内注射Aβ25-35可导致大鼠空间学习记忆功能障碍;联合实验中Aβ25-35同样可引起在体海马LTP改变。提示同批动物先后进行行为学和电生理学测试的方法是可行的,行为学实验不会影响后续LTP的实验结果。因此,本实验为行为学改变后进行在体LTP机制探讨提供了实验依据,为有效开展行为学和电生理学实验提供了思路。展开更多
基金supported by the National Basic Research Program of China(No.2002CB512907)the National Natural Science Foundation of China(No.30630057).
文摘Objective To explore the changes in spatial learning performance and long-term potentiation(LTP)which is recognized as a component of the cellular basis of learning and memory in normal and lead-exposed rats after administration of melatonin (MT)for two months.Methods Experiment was performed in adult male Wistar rats(12 controls,12 exposed to melatonin treatment,10 exposed to lead and 10 exposed to lead and melatonin treatment).The lead-exposed rats received 0.2%lead acetate solution from their birth day while the control rats drank tap water.Melatonin(3 mg/kg)or vehicle was administered to the control and lead-exposed rats from the time of their weaning by gastric gavage each day for 60 days,depending on their groups.At the age of 81-90 days.all the animals were subjected to Morris water maze test and then used for extracellular recording of LTP in the dentate gyrus(DG)area of the hippocampus in vivo.Results Low dose of melatonin given from weaning for two months impaired LTP in the DG area of hippocampus and induced learning and memory deficit in the control rats.When melatonin was administered over a prolonged period to the lead-exposed rats,it exacerbated LTP impairment.learning and memory deficit induced by lead.Conclusion Melatonin is not suitable for normal and lead-exposed children.
文摘目的:探讨海马内注射β-amyloid protein 25-35(Aβ25-35)所致Alzheizer’s病(AD)模型大鼠空间学习记忆功能障碍的海马突触可塑性长时程增强(LTP)机制,为联合开展AD动物行为学和在体电生理学研究提供实验证据。方法:在脑立体定位仪上给予大鼠双侧海马分别注射4 nmol/L Aβ25-35或等体积生理盐水每侧2μl,手术后恢复2周,每只大鼠依次进行行为学和电生理两部分实验。首先,利用Morris水迷宫进行空间学习、记忆功能测试;之后,进行在体海马CA1区场兴奋性突触后电位(fEPSP)引导记录实验,观察突触可塑性指标长时程增强(LTP)的改变。结果:与对照组相比,海马内注射Aβ25-35大鼠的空间学习记忆功能和在体海马突触可塑性LTP均有改变,其中:逃避潜伏期和逃避距离明显增加(P<0.01);目标象限内游泳时间和距离明显缩短(P<0.01);在体海马LTP幅度显著降低(P<0.01)。结论:海马内注射Aβ25-35可导致大鼠空间学习记忆功能障碍;联合实验中Aβ25-35同样可引起在体海马LTP改变。提示同批动物先后进行行为学和电生理学测试的方法是可行的,行为学实验不会影响后续LTP的实验结果。因此,本实验为行为学改变后进行在体LTP机制探讨提供了实验依据,为有效开展行为学和电生理学实验提供了思路。
