Vanillic acid attenuates amyloid β1-40-induced long-term potentiation deficit in male rats: an in vivo investigation

ABSTRACT

Objectives: Alzheimer disease (AD) is a neurodegenerative disorderliness that involves deductible progressive cognition function caused by amyloid-beta (Aβ) peptide accumulation in the interstitial space. The increase of Aβ stimulates all kinds of active oxygen and causes oxidative stress and apoptosis. In this investigation, we researched the neuroprotective impacts of vanillic acid (VA) on the Aβ-induced (Aβ1-40) long-term potentiation (LTP) of the hippocampus – a commonly probed synaptic plasticity model that happens at the same time as memory and learning – in the AD rats.

Methods: Forty-five male Wistar rats were categorized into five groups (n = 8 rats/group, 200–220 g), and studied as control (standard diet), sham (vehicle), VA (50 mg/kg), Aβ and Aβ + VA (50 mg/kg) groups. In vivo electrophysiological recordings were implemented after the stereotaxic surgery to gauge the excitatory postsynaptic potential (EPSP) slope and population spike (PS) amplitude in the dentate gyrus of the hippocampus. By the stimulation at high-frequency of the perforate pathway, long-term potentiation (LTP) was induced. To assess the plasma levels of malondialdehyde (MDA) and total thiol group (TTG), blood samples were garnered.

Results: In the Aβ-injected rats, EPSP slope, and PS amplitude were significantly reduced after the induction of LTP. Thus, the findings demonstrate that VA decreases the impacts of Aβ on LTP; also, the treatments through VA neuroprotective against the negative effects of Aβ on the synaptic plasticity of the hippocampus can decrease the MDA levels and also increase the TTG levels significantly.

Discussion: Therefore, based on this experiment on male rats, VA has neuroprotective effects and antioxidants benefits against the Aβ-mediated inhibition of long-term potentiation.

KEYWORDS:

• Vanillic acid
• hippocampus
• Alzheimer disease
• β-amyloid
• long-term potentiation
• rats

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Notes on contributors

Nesa Ahmadi

Nesa Ahmadi M.Sc., Department of Biology, Faculty of Basic Sciences, Bu-Ali Sina University.

Naser Mirazi

Naser Mirazi Professor, Department of Biology, Faculty of Basic Sciences, Bu-Ali Sina University.

Alireza Komaki

Alireza Komaki Professor, Neurophysiology Research Center, Hamedan University of Medical Sciences.

Samaneh Safari

Samaneh Safari M.Sc., Department of Biology, Faculty of Basic Sciences, Bu-Ali Sina University.

Abdolkarim Hosseini

Abdolkarim Hosseini Ph.D., Department of Animal Sciences and Biotechnology, Faculty of Life Sciences and Biotechnology, Shahid Beheshti University.