Author(s): Jing W, Guo F, Cheng L, Zhang JF, Qi JS
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Abstract Amyloid beta protein (Abeta) is thought to be responsible for the loss of memory in Alzheimer's disease (AD). A significant decrease in [Arg(8)]-vasopressin (AVP) in the AD brain has been found. However, it is unclear whether the decrease in AVP is involved in Abeta-induced impairment of memory and whether AVP can protect against Abeta-induced neurotoxicity. The present study examines the effects of intracerebroventricular (i.c.v.) injection of AVP on hippocampal long-term potentiation (LTP), a synaptic model of memory, and investigates the potential protective function of AVP in Abeta-induced LTP impairment. The results showed that (1) i.c.v. injection of different concentrations of AVP or Abeta(25-35) did not affect the baseline field excitatory postsynaptic potentials (fEPSPs); (2) AVP administration alone induced a significant increase in HFS-induced LTP, while Abeta(25-35) significantly suppressed HFS-induced LTP; (3) Abeta(25-35)-induced LTP suppression was significantly prevented by the pretreatment with AVP; (4) paired-pulse facilitation did not change after separate application or co-application of AVP and Abeta(25-35). These results indicate that AVP can potentiate hippocampal synaptic plasticity and dose-dependently prevent Abeta(25-35)-induced LTP impairment. Thus, the present study provides further insight into the mechanisms by which Abeta impairs synaptic plasticity and suggests an important approach in the treatment of AD.
This article was published in Neurosci Lett
and referenced in Journal of Alzheimers Disease & Parkinsonism