Effects of Vanillic acid on hippocampal synaptic plasticity in male rats with Alzheimer’s disease induced by β-amyloid

Background and Aim : Alzheimer s disease (AD) is a neurodegenerative disorder characterized by a progressive decline in cognitive function, due to the accumulation of beta-amyloid peptide (Aβ) in the extracellular space. Aβ stimulates the production of active oxygen species and thus leads to oxidative stress and cell death. Vanillic Acid (VA) has many properties such as suppressing apoptosis and removes the harmful effects of oxidative stress on synaptic plasticity. Therefore, in the present study, we examined the therapeutic effect of VA on Aβ-induced impairments in the hippocampal synaptic plasticity in AD model rats.Methods : Our experiments were conducted on 40 male Wistar rats randomly assigned to 5 groups (n = 8): control, sham (intraventricular saline injections), AD (Aβ; intraventricular Aβ injections), VA treatment (50 mg/kg) and AD with VA treatment. Rats were injected with Aβ to induce AD, allowed to recover, and treated with VA for 4 weeks. The rats were then anesthetized with intraperitoneal injections of urethane and placed in a stereotaxic apparatus for surgery, electrode implantation, and field potential recording. In vivo electrophysiological recordings were then performed to measure population spike (PS) amplitude and excitatory postsynaptic potential (EPSP) slope in the hippocampal dentate gyrus. Long-term potentiation (LTP) was induced by high-frequency stimulation of the perforant pathway. Statistical significance was set at p≤0.05.Results : Rats that received A exhibited a significant decrease in their EPSP slope and PS amplitude as compared to the control group. In contrast, VA administration in the AD + VA rats reduced the increase in the EPSP slope and PS amplitude.Conclusion : VA decreased the Aβ-induced synaptic plasticity impairments in AD rats. Therefore, these results suggest that VA, a natural antioxidant, can be therapeutic agent, against high risk factors for AD, such as oxidative stress.

کلیدواژه ها:

Vanillic acid ، Alzheimer’s disease ، Rat ، Synaptic plasticity ، Long term potentiation