Arginine vasopressin remolds the spontaneous discharges disturbed by amyloid β protein in hippocampal CA1 region of rats

Beta-amyloid peptide (A beta) aggregated in the brain is the main pathological characteristic of Alzheimer's disease (AD), and a significant decrease in the concentration of arginine vasopressin (AVP) in the brain of AD patients has been reported. Our recent study shows that intracerebroventricular (i.c.v.) injection of AVP protects against A beta-induced impairments of spatial learning and memory. However, it is still unclear whether the A beta-induced cognitive deficit is involved in the alteration of central neuronal discharges, and further whether AVP can modulate the electrophysiological change induced by A beta. The present study thus observed the effects of AVP, A beta and AVP plus A beta on the spontaneous discharges of hippocampal CA1 neurons in rats by using multi-channel extracellular recording technique. The results showed that: (1) the average frequency of spontaneous discharges was decreased by i.c.v. injection of 25 nmol A beta(25-35); (2) 10 nmol AVP induced an increase in spike discharge in the hippocampal CA1 neurons: (3) pretreatment with 10 nmol AVP effectively reversed A beta(25-35) induced suppression of spontaneous discharges in hippocampal CA1 region. These in vivo electrophysiological results indicate that AVP, as a hormone and neurotransmitter, can remold the spontaneous discharges disturbed by A beta and counteract the deleterious effect of A beta(25-35) on neural circuit, suggesting that the activation of central vasopressinergic system may play a beneficial role for the prevention and treatment of cognitive impairments in AD. (C) 2013 Elsevier B.V. All rights reserved.