Volume 7, Issue 2 (Spring 2016 -- 2016)                   BCN 2016, 7(2): 97-106 | Back to browse issues page

PMID: 27303604


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1- Physiology Research Center, Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
2- Department of Biology, Science & Research Branch, Islamic Azad University, Tehran, Iran.
3- Department of Pathology, Faculty of Specialized Veterinary Science, Science & Research Branch, Islamic Azad University, Tehran, Iran.
4- Department of Nursing and Midwifery, Dezfoul Branch, Islamic Azad University, Dezfoul, Iran.
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.

Type of Study: Original | Subject: Cognitive Neuroscience
Received: 2015/04/24 | Accepted: 2015/09/1 | Published: 2016/04/1

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