Document Type: Research article
Neuroscience Research Center, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Department of Physiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
It has been shown that brain glucose metabolism impairment, obesity, and diabetes could
lead to cognitive decline and Alzheimer’s disease (AD) pathogenesis. Kisspeptin (KP) a G-protein
coupled receptor neuropeptide, has been suggested as a link between energy balance and
reproduction. Some studies have shown that the attenuation of KP signaling decreases metabolism
and energy expenditure. KP mRNAs and receptors are detected in the hippocampus
and cause the promotion of excitatory synaptic responses through modulation of postsynaptic
signaling. The purpose of this study was to investigate the effect of KP on spatial learning and
memory and its possible neuroprotective effect on Amyloid-Beta induced cognitive impairment
using the Morris Water Maze (MWM) task in rats. The reference and reversal spatial learning
and memory have been measured in this study. Rats were injected bilaterally by Aβ1-42 (2 μg/
μL) or saline as a vehicle into the hippocampal CA1 area. One week later, KP-13 (1.5 or 2 μg/
μL) was injected i.c.v before or after each training session for 3 days and memory was tested
24 h later. The results showed KP-13 by itself could significantly enhance spatial memory
consolidation and retrieval, and Aβ induced reversal and reference memory impairment was
significantly ameliorated by KP-13. In Conclusion, it seems that KP-13 as a neuropeptide has
to enhance spatial memory properties and could be a possible neuroprotective peptide on amyloid-
beta induced pathology.