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

Amyloid β protein (Aβ) is thought to be responsible for the loss of memory in Alzheimer's disease (AD). A significant decrease in [Arg8]-vasopressin (AVP) in the AD brain has been found. However, it is unclear whether the decrease in AVP is involved in Aβ-induced impairment of memory and whether AVP can protect against Aβ-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 Aβ-induced LTP impairment. The results showed that (1) i.c.v. injection of different concentrations of AVP or Aβ25–35 did not affect the baseline field excitatory postsynaptic potentials (fEPSPs); (2) AVP administration alone induced a significant increase in HFS-induced LTP, while Aβ25–35 significantly suppressed HFS-induced LTP; (3) Aβ25–35-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 Aβ25–35. These results indicate that AVP can potentiate hippocampal synaptic plasticity and dose-dependently prevent Aβ25–35-induced LTP impairment. Thus, the present study provides further insight into the mechanisms by which Aβ impairs synaptic plasticity and suggests an important approach in the treatment of AD.