Arginine vasopressin prevents amyloid β protein-induced impairment of long-term potentiation in rat hippocampus in vivo

Amyloid beta protein (A beta) 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 A beta-induced impairment of memory and whether AVP can protect against A beta-induced neurotoxicity. The present study examines the effects of intracerebroventricular (i.c.v.) injection of AVP on hippocampal long-term potentiation (UP), a synaptic model of memory. and investigates the potential protective function of AVP in A beta-induced LTP impairment. The results showed that (I) i.c.v. injection of different concentrations of AVP or A beta(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 A beta(25-35) significantly suppressed HFS-induced LTP; (3) A beta(25-35)-induced UP 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 A beta(25-35). These results indicate that AVP can potentiate hippocampal synaptic plasticity and dose-dependently prevent A beta(25-35)-induced UP impairment. Thus, the present study provides further insight into the mechanisms by which A beta impairs synaptic plasticity and suggests an important approach in the treatment of AD. (C) 2008 Elsevier Ireland Ltd. All rights reserved.