Effect of troxerutin on synaptic plasticity of hippocampal dentate gyrus neurons in a β-amyloid model of Alzheimer׳s disease: An electrophysiological study

• DOI: 10.1016/j.ejphar.2014.03.018
• Publication Date: 2014-03-25T17:49:01Z
• Authors: Shirin Babri; Gisou Mohaddes; Iraj Feizi; Alireza Mohammadnia; Ali Niapour; Alireza Alihemmati; Mohammad Amani
• Keywords: Male; 0301 basic medicine; Memory Disorders; Amyloid beta-Peptides; Neuronal Plasticity; Long-Term Potentiation; Electrophysiological Phenomena; Rats; 3. Good health; Hydroxyethylrutoside; 03 medical and health sciences; Neuroprotective Agents; Alzheimer Disease; Dentate Gyrus; Synapses; Animals; Rats, Wistar; Maze Learning

Alzheimer׳s disease (AD) is a neurodegenerative disorder with a progressive cognitive decline and memory loss. Multiple pathogenetic factors including aggregated β-amyloid (Aβ), neurofibrillary tangles (NFTs), cholinergic dysfunction and oxidative stress are involved in AD. Aβ, a major constituent of the senile plaques, is a potent neurotoxic peptide and has a pivotal role in cognitive deficit and reduced synaptic plasticity in AD. In the present study we examined the protective effect of troxerutin, as a multipotent bioflavonoid, on Aβ (1-42)-induced impairment of evoked field potential in hippocampal DG neurons. Male Wistar rats were divided into four groups including Aβ (42-1), Aβ (1-42), Aβ (1-42) plus troxerutin and Aβ (42-1) plus troxerutin groups. Aβ was injected intracerebroventricularly (i.c.v.) into right lateral ventricle and after two weeks the evoked field potential recorded from perforant path-DG synapses to assess paired pulse paradigm and long term potentiation (LTP). Administration of Aβ (1-42) drastically attenuated the LTP of DG neurons, while there was no significant difference in evoked field potentials between Aβ (1-42) plus troxerutin group with respect to Aβ (42-1) group. This study revealed that troxerutin improves the synaptic failure induced by Aβ peptide and can be introduced as a promising multi-potent pharmacological agent in prevention or treatment of AD in the future.