Author/Authors :
Hajipour، Somayeh نويسنده Physiology Research Center, Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. Hajipour, Somayeh , SARKAKI، ALIREZA نويسنده , , Farbood، Yaghoob نويسنده Ahvaz Jundishapur University of Medical Sciences (AJUMS), School of Medicine, Department of Physiology, Physiology Research Center, Ahvaz, I.R. Iran Farbood, Yaghoob , Eidi، Akram نويسنده Department of Biology‚ Science & Research Branch , , Mortazavi، Pejman نويسنده , , Valizadeh، Zohreh نويسنده Department of Nursing and Midwifery, Dezfoul Branch, Islamic Azad University, Dezfoul, Iran. Valizadeh, Zohreh
Abstract :
Introduction: To study the effect of gallic acid (GA) on hippocampal long-term potentiation (LTP) and histological changes in animal model of Alzheimer disease (AD) induced by betaamyloid (Aβ).
Methods: Sixty-four adult male Wistar rats (300±20 g) were divided into 8 groups: 1) Control (Cont); 2) AD; 3) Sham; 4-7) AD+GA (50, 100, and 200 mg/kg for 10 days, orally) or vehicle, 8) Cont+GA100, Aβ (1μg/μL in each site) was infused into hippocampus bilaterally. Changes of amplitude and slope of LTP induced in hippocampal dentate gyrus (DG) were evaluated by high frequency stimulation (HFS) of perforant path (PP).
Results: Data showed that LTP amplitude and area under curve significantly impaired in AD rats (P<0.001), while significantly improved in AD rats treated with GA (P<0.05, P<0.01).
Conclusion: Current findings suggest that GA reduces neural damage and brain amyloid neuropathology and improves cognitive function via free radicals scavenging and inhibiting oligomerization of Aβ but with no effect on healthy rats.
