کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1904548 | 1534640 | 2015 | 41 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Fructose consumption reduces hippocampal synaptic plasticity underlying cognitive performance
ترجمه فارسی عنوان
مصرف فروکتوز پلاستیک سیناپسی هیپوکامپ را پایین می آورد و عملکرد شناختی را تحت تاثیر قرار می دهد
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کلمات کلیدی
4-HNEPostsynaptic densitiesPSDsSGZGluTsPTXMWMfEPSPGCLCBFaCSF4-hydroxynonenalNeuronal dysfunction - اختلال عملکرد نورونlong-term depression - افسردگی طولانی مدتAlzheimer's disease - بیماری آلزایمرDiabetes - بیماری قندlong-term potentiation - تقویت درازمدتLTP - تقویت طولانی مدت یا LTP cerebral blood flow - جریان خون مغزیglucose transporters - حمل و نقل گلوکزMetabolic syndrome - سندرم متابولیکFructose - فروکتوز granule cell layer - لایه سلول گرانولMorris water maze - ماز آب آب موریسartificial cerebro-spinal fluid - مایع مغزی نخاعی مغزیMETS - متسLTD - محدودField excitatory postsynaptic potential - پتانسیل پستنیپتیک مزمن تحریک پذیرPicrotoxin - پیکروتوکسین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
چکیده انگلیسی
Metabolic syndrome (MetS) is a global epidemic, which involves a spectrum of metabolic disorders comprising diabetes and obesity. The impact of MetS on the brain is becoming to be a concern, however, the poor understanding of mechanisms involved has limited the development of therapeutic strategies. We induced a MetS-like condition by exposing mice to fructose feeding for 7Â weeks. There was a dramatic deterioration in the capacity of the hippocampus to sustain synaptic plasticity in the forms of long-term potentiation (LTP) and long-term depression (LTD). Mice exposed to fructose showed a reduction in the number of contact zones and the size of postsynaptic densities (PSDs) in the hippocampus, as well as a decrease in hippocampal neurogenesis. There was an increase in lipid peroxidation likely associated with a deficiency in plasma membrane excitability. Consistent with an overall hippocampal dysfunction, there was a subsequent decrease in hippocampal dependent learning and memory performance, i.e., spatial learning and episodic memory. Most of the pathological sequel of MetS in the brain was reversed three month after discontinue fructose feeding. These results are novel to show that MetS triggers a cascade of molecular events, which disrupt hippocampal functional plasticity, and specific aspects of learning and memory function. The overall information raises concerns about the risk imposed by excessive fructose consumption on the pathology of neurological disorders.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1852, Issue 11, November 2015, Pages 2379-2390
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1852, Issue 11, November 2015, Pages 2379-2390
نویسندگان
Pedro Cisternas, Paulina Salazar, Felipe G. Serrano, Carla Montecinos-Oliva, Sebastián B. Arredondo, Lorena Varela-Nallar, Salesa Barja, Carlos P. Vio, Fernando Gomez-Pinilla, Nibaldo C. Inestrosa,