Effect of troxerutin on synaptic plasticity of hippocampal dentate gyrus neuronsina beta-amyloid model of Alzheimer's disease: An electrophysiological study

Abstract

Alzheimer's disease(AD) is a neurodegenerative disorder with a progressive cognitive decline and memory loss. Multiple pathogenetic factors including aggregated beta-amyloid(A beta), neurofibrillary tangles (NFTs), cholinergic dysfunction and oxidative stress are involved in AD. A beta, a major constituent of the senile plaques, is a potent neurotoxic peptide and has a pivotal role incognitive deficit and reduced synaptic plasticity in AD. In the present study we examined the protective effect of troxerutin, as a multipotent bioflavonoid, on A beta (1-42)-induced impairment of evoked field potential in hippocampal DG neurons. Male Wistar rats were divided into four groups including A beta (42-1), A beta (1-42), A beta (1-42) plus troxerutin and A beta (42-1) plus troxerutin groups. A beta 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 A beta (1-42) drastically attenuated the LTP of DG neurons, while there was no significant difference in evoked field potentials between A beta (1-42) plus troxerutin group with respect to A beta (42-1) group. This study revealed that troxerutin improves the synaptic failure induced by A beta peptide and can be introduced as a promising multi-potent pharmacological agent in prevention or treatment of AD in the future. (C) 2014 Elsevier B.V. All rights reserved.