A specific multi-nutrient enriched diet enhances hippocampal cholinergic transmission in aged rats

NEUROBIOLOGY OF AGING

卷:36

Article

Cansev, Mehmet¹  van Wijk, Nick²  Turkyilmaz, Mesut¹  Orhan, Fulya¹  Sijben, John W. C.²  Broersen, Laus M.² 

[1] Uludag Univ, Sch Med, Dept Pharmacol, TR-16059 Bursa, Turkey

[2] Nutr Res, Nutr Adv Med Nutr, Utrecht, Netherlands

关键词: Alzheimer's disease;    Fortasyn connect;    Souvenaid;    Acetylcholine release;    Cholinergic neurotransmission;    Phospholipid;    Synaptic membrane;    Choline acetyltransferase;    Aged rat;   

DOI  :  10.1016/j.neurobiolaging.2014.07.021

来源: Elsevier

【 摘 要 】

Fortasyn Connect (FC) is a specific nutrient combination designed to target synaptic dysfunction in Alzheimer's disease by providing neuronal membrane precursors and other supportive nutrients. The aim of the present study was to investigate the effects of FC on hippocampal cholinergic neurotransmission in association with its effects on synaptic membrane formation in aged rats. Eighteen-month-old male Wistar rats were randomized to receive a control diet for 4 weeks or an FC-enriched diet for 4 or 6 weeks. At the end of the dietary treatments, acetylcholine (ACh) release was investigated by in vivo microdialysis in the right hippocampi. On completion of microdialysis studies, the rats were sacrificed, and the left hippocampi were obtained to determine the levels of choline, ACh, membrane phospholipids, synaptic proteins, and choline acetyltransferase. Our results revealed that supplementation with FC diet for 4 or 6 weeks, significantly enhanced basal and stimulated hippocampal ACh release and ACh tissue levels, along with levels of phospholipids. Feeding rats the FC diet for 6 weeks significantly increased the levels of choline acetyltransferase, the presynaptic marker Synapsin-1, and the postsynaptic marker PSD-95, but decreased levels of Nogo-A, a neurite outgrowth inhibitor. These data show that the FC diet enhances hippocampal cholinergic neurotransmission in aged rats and suggest that this effect is mediated by enhanced synaptic membrane formation. These data provide further insight into cellular and molecular mechanisms by which FC may support memory processes in Alzheimer's disease. (C) 2015 The Authors. Published by Elsevier Inc. All rights reserved.

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