Brain-derived neurotrophic factor prevents against amyloid beta protein-induced impairment of hippocampal in vivo long-term potentiation in rats / 中国应用生理学杂志

ABSTRACT

<p><b>OBJECTIVE</b>To explore the effects of brain-derived neurotrophic factor (BDNF) pretreatment on beta amyloid protein (Abeta) induced impairment of in vivo hippocampal long-term potentiation (LTP) in the CA1 region of rats.</p><p><b>METHODS</b>Thirty-six adult male SD rats were randomly divided into six groups (n = 6): control, Abeta25-35, BDNF, (0.02 microg, 0.1 microg, 0.5 microg) BDNF + Abeta25-35. 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.</p><p><b>RESULTS</b>(1) Abeta25-35 (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 microg) alone did not affect the baseline fEPSPs and HFS-induced LTP. (3) Compared with Abeta25-35 alone group, the averaged amplitude of LTP in BDNF (0.1 microg and 0.5 microg) plus Abeta25-35 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 Abeta,25-35 induced depression of LTP in a dose-dependent manner.</p><p><b>CONCLUSION</b>Intrahippocampal injection of BDNF can protect against the Abeta25-35-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.</p>