Author(s): Pan YF, Jia XT, Wang XH, Chen XR, Li QS,
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Abstract Beta-amyloid peptide (Aβ) 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 Aβ-induced impairments of spatial learning and memory. However, it is still unclear whether the Aβ-induced cognitive deficit is involved in the alteration of central neuronal discharges, and further whether AVP can modulate the electrophysiological change induced by Aβ. The present study thus observed the effects of AVP, Aβ and AVP plus Aβ 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 Aβ(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 Aβ(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 Aβ and counteract the deleterious effect of Aβ(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. Copyright © 2013 Elsevier B.V. All rights reserved.
This article was published in Regul Pept
and referenced in Journal of Alzheimers Disease & Parkinsonism