中文摘要：

目的：探讨脑源性神经营养因子（BDNF）对β淀粉样蛋白（Aβ）致大鼠突触功能障碍的保护作用。方法：36只健康雄性SD大鼠随机分为对照、Aβ25-35、BDNF、不同剂量BDNF（0.02μg,0.1μg,0.5μg）＋Aβ25-35等六组（n=6）。实验采用电生理学手段,利用自制的海马给药装置和刺激/记录绑定电极引导和记录大鼠在体海马CA1区场兴奋性突触后电位（fEPSPs）和高频刺激（HFS）诱导的长时程增强（LTP）。结果：①海马CA1区注射Aβ25-35（2 nmol）不影响基础性fEPSPs,但能显著抑制LTP的诱导与维持,HFS后fEPSPs平均幅度较对照组明显降低（P〈0.01）;②海马CA1区注射BDNF（0.1μg）不影响基础性fEPSPs,也不影响LTP的诱导与维持,HFS后fEPSPs平均幅度与对照组相比没有明显差异（P〉0.05）;③与单独给予Aβ25-35相比,不同浓度的BDNF（0.1μg,0.5μg）与Aβ25-35合用组在HFS后0 min、30 min和60 min时的fEPSPs平均幅度均明显增加（P〈0.01）,并具有一定的剂量依赖性,表明BDNF预处理可有效拮抗Aβ25-35引起的LTP抑制。结论：脑内注射BDNF能够预防和拮抗由Aβ25-35引起的海马LTP损伤,提示BDNF水平的上调有助于维持正常的突触可塑性并可能改善AD患者的学习记忆功能。

英文摘要：

Objective： To explore the effects of brain-derived neurotrophic factor（BDNF） pretreatment on β amyloid protein（Aβ）induced impairment of in vivo hippocampal long-term potentiation（LTP）in the CA1 region of rats.Methods： Thiyty-six adult male SD rats were randomly divided into six groups（n=6）： control,Aβ25-35,BDNF,（0.02 μg,0.1 μg,0.5 μg） BDNF＋Aβ25-35.A self-made hippocampal local drug delivery catheter and a parallel bound stimulating/recording electrode were used to deliver drugs/stimulation and record field excitatory post-synaptic potentials（fEPSPs） in the hippocampal CA1 region of rats.High-frequency stimulation（HFS） was used to induce in vivo LTP.Results： ① Aβ25-35（2 nmol） injection into CA1 region of rats did not affect the baseline fEPSPs,but inhibited the HFS-induced LTP significantly（P〈0.01）.② Hippocampal CA1 injection of BDNF（0.1 μg） alone did not affect the baseline fEPSPs and HFS-induced LTP.③ Compared with Aβ25-35 alone group,the averaged amplitude of LTP in BDNF（0.1 μg and 0.5 μg） plus Aβ25-35 groups significantly increased at 0 min,30 min,and 60 min after HFS（P〈0.01）,indicating that pretreatment with BDNF effectively protected against the Aβ25-35 induced depression of LTP in a dose-dependent manner.Conclusion： Intrahippocampal injection of BDNF can protect against the Aβ25-35-induced LTP impairment,suggesting that the up-regulation of BDNF in the brain could maintain the normal hippocampal synaptic plasticity and may contribute to the improvement of learning and memory in Alzheimer’s（AD） disease patients.