Effect of Gallic Acid on Dementia Type of Alzheimer Disease in Rats: Electrophysiological and Histological Studies

• Published in: Basic and clinical neuroscience Vol. 7; no. 2; pp. 97 - 106
• Main Authors: Hajipour, S., Sarkaki, A., Farbood, Y., Eidi, A., Mortazavi, P., Valizadeh, Z.
• Format: Journal Article
• Language: English
• Published: Iran Negah Scientific Publisher 01.04.2016; Iranian Neuroscience Society; Iran University of Medical Sciences
• Subjects: Alzheimer disease; Alzheimer's disease; Beta-amyloid; Brain injury; Cognitive ability; Dementia; Dementia disorders; Dentate gyrus; Free radicals; Gallic acid; Hippocampus; Long-term potentiation; Neurodegenerative diseases; Neuronal apoptosis; Oligomerization; Rat; Research Papers; Rodents; Neuronal apoptosis; Rat; Alzheimer disease; Long-term potentiation; Beta-amyloid
• ISSN: 2228-7442; 2008-126X; 2228-7442
• DOI: 10.15412/J.BCN.03070203

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 beta-amyloid (Aβ). 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). 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). 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.