PMID- 23252296
OWN - NLM
STAT- MEDLINE
DCOM- 20140123
LR  - 20121220
IS  - 1000-6834 (Print)
IS  - 1000-6834 (Linking)
VI  - 28
IP  - 5
DP  - 2012 Sep
TI  - [Brain-derived neurotrophic factor prevents against amyloid beta protein-induced 
      impairment of hippocampal in vivo long-term potentiation in rats].
PG  - 425-9
AB  - OBJECTIVE: 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. METHODS: 
      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. 
      RESULTS: (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. CONCLUSION: 
      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.
FAU - Li, Qing-Shan
AU  - Li QS
AD  - The Second Affiliated Hospital of Shan Xi Medical University, Taiyuan 030001, 
      China.
FAU - Yang, Wei
AU  - Yang W
FAU - Pan, Yan-Fang
AU  - Pan YF
FAU - Min, Jie
AU  - Min J
FAU - Zhang, Zhe
AU  - Zhang Z
FAU - Gao, Hui-Zhong
AU  - Gao HZ
FAU - Qi, Jin-Shun
AU  - Qi JS
LA  - chi
PT  - English Abstract
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - China
TA  - Zhongguo Ying Yong Sheng Li Xue Za Zhi
JT  - Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = 
      Chinese journal of applied physiology
JID - 9426407
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Peptide Fragments)
RN  - 0 (amyloid beta-protein (25-35))
SB  - IM
MH  - Amyloid beta-Peptides/*antagonists & inhibitors
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*pharmacology
MH  - CA1 Region, Hippocampal/*drug effects/*physiology
MH  - Excitatory Postsynaptic Potentials/physiology
MH  - Long-Term Potentiation/*physiology
MH  - Male
MH  - Peptide Fragments/*antagonists & inhibitors
MH  - Rats
MH  - Rats, Sprague-Dawley
EDAT- 2012/12/21 06:00
MHDA- 2014/01/24 06:00
CRDT- 2012/12/21 06:00
PHST- 2012/12/21 06:00 [entrez]
PHST- 2012/12/21 06:00 [pubmed]
PHST- 2014/01/24 06:00 [medline]
PST - ppublish
SO  - Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2012 Sep;28(5):425-9.