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

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• 作者：Shirin Babri^a ; ¹ ; Gisou Mohaddes^b ; Iraj Feizi^c ; Alireza Mohammadnia^d ; Ali Niapour^e ; Alireza Alihemmati^f ; Mohammad Amani^g ; ¹ ; ^{mohammad.amani@arums.ac.ir" class="auth_mail}
• 关键词：Troxerutin ; Synaptic plasticity ; 尾-Amyloid ; Dentate gyrus ; Alzheimer壮s disease
• 刊名：European Journal of Pharmacology
• 出版年：5 June 2014
• 年：2014
• 卷：732
• 期：Complete
• 页码：19-25
• 全文大小：995 K

文摘

Alzheimer壮s disease (AD) is a neurodegenerative disorder with a progressive cognitive decline and memory loss. Multiple pathogenetic factors including aggregated 尾-amyloid (A尾), neurofibrillary tangles (NFTs), cholinergic dysfunction and oxidative stress are involved in AD. A尾, 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 A尾 (1–42)-induced impairment of evoked field potential in hippocampal DG neurons. Male Wistar rats were divided into four groups including A尾 (42–1), A尾 (1–42), A尾 (1–42) plus troxerutin and A尾 (42–1) plus troxerutin groups. A尾 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尾 (1–42) drastically attenuated the LTP of DG neurons, while there was no significant difference in evoked field potentials between A尾 (1–42) plus troxerutin group with respect to A尾 (42–1) group. This study revealed that troxerutin improves the synaptic failure induced by A尾 peptide and can be introduced as a promising multi-potent pharmacological agent in prevention or treatment of AD in the future.