کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6809167 | 1433595 | 2012 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Rescue of cognitive aging by long-lasting environmental enrichment exposure initiated before median lifespan
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کلمات کلیدی
PFVTBSD-APVAMPA-RaCSFNBQXNMDA-RMWMfEPSPPPFStandard conditionsd-2-amino-5-phosphonovalerate - d-2-amino-5-fosfonovalerateNMDA receptor - NMDA گیرندهpaired-pulse facilitation - تسکین زوایای پالسیlong-term potentiation - تقویت درازمدتLTP - تقویت طولانی مدت یا LTP Memory - حافظهCognitive reserve - ذخیره شناختیLifespan - طول عمرEnvironmental enrichment - غنی سازی محیط زیستMorris water maze - ماز آب آب موریسartificial cerebrospinal fluid - مایع مغزی نخاعی مصنوعیHippocampus - هیپوکامپ field excitatory postsynaptic potentials - پتانسیل پستنیپتیک تحریک پذیری میدانSynaptic plasticity - پلاستیسیته سیناپسیN-methyl-d-aspartate receptor - گیرنده N-methyl-d-aspartateLearning - یادگیری
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The rescue of cognitive function through environmental enrichment (EE) during aging has been extensively documented. However, the age at onset, the duration of EE, and the cerebral mechanisms required to obtain the greatest benefits still remain to be determined. We have recently shown that EE applied for 3 mo after the median lifespan, i.e., the age at which 50% of the population is still alive (from 17 to 20 mo in NMRI mice), failed to prevent cognitive deficits in senescent animals. In the present study, mice were exposed to EE prior to the median lifespan, and for a longer total duration (from 14 to 20 mo), before the assessment of memory performance and the electrophysiological properties of hippocampal neuronal networks. The EE prevented memory deficits and reduced anxiety as the animal aged. Moreover, EE attenuated the age-related impairment of basal glutamatergic neurotransmission in CA1 hippocampal slices, and reversed the decrease in isolated N-methyl-D-Aspartate receptor (NMDA-R)-dependent synaptic potentials. Surprisingly, EE did not prevent the age-related alteration of theta-burst-induced long-term potentiation (LTP). This study therefore suggests that EE needs to be initiated before the age corresponding to the median lifespan and/or required long duration (> 3 mo) to have an effect on cognitive aging. In addition, we show that EE probably acts through theta-burst-independent mechanisms of synaptic plasticity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Aging - Volume 33, Issue 5, May 2012, Pages 1005.e1-1005.e10
Journal: Neurobiology of Aging - Volume 33, Issue 5, May 2012, Pages 1005.e1-1005.e10
نویسندگان
T. Freret, J.-M. Billard, P. Schumann-Bard, P. Dutar, F. Dauphin, M. Boulouard, V. Bouet,