Introduction: Brain-derived neurotrophic factor (BDNF) improved the spatial learning and memory impaired by accumulated β amyloid protein (Aβ) 25-35, to explore BDNF protection mechanism whether to change the synaptic plasticity in hippocampus.Methods: A self-made hippocampal local drug delivery catheter and a parallel bound stimulating/recording electrode were used to deliver drugs/stimulation and record in vivo hippocampal long-term potentiation(LTP)in the CA 1 region of rats.Results: (1)Aβ2s-35 (2 nmol) alone did not affect the baseline field excitatory post-synaptic potentials (fEPSPs), but significantly inhibited the high-frequency stimulation (HFS)-induced LTP (P<0.01).(2) BDNF (0.1 μg) alone did not affect the baseline fEPSPs and HFSinduced LTP (3) Compared with Aβ25-35 alone group, the averaged amplitude of LTP in BDNF (0.1 μg and 0.5μg) plus Aβ25-35 groups significantly increased at 0 min, 30 min, and 60 min after HFS (P<0.01), indicating that BDNF 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 nemory in AD patients.