کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6277446 | 1295759 | 2009 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Cellular prion protein modulates age-related behavioral and neurochemical alterations in mice
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کلمات کلیدی
Gerstmann-Straüssler-ScheinkerSTI1PRNPDABPBSTNBPrPcCellular prion protein (PrPC)GSSpKaLTMDTNBSTM3,3′-diaminobenzidine - 3،3'-diaminobenzidineMAPK - MAPKAChE - آهیAcetylcholinesterase - استیل کولین استرازAcetylcholinesterase (AChE) - استیل کولین استراز (AChE)Alzheimer's disease - بیماری آلزایمرParkinson's disease - بیماری پارکینسونanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of variancelong-term potentiation - تقویت درازمدتLTP - تقویت طولانی مدت یا LTP long-term memory - حافظه بلندمدتshort-term memory - حافظه کوتاه مدتBehavior - رفتارAging - سالخوردگیSynaptophysin - سیناپتوفیزینdentate gyrus - شکنج دندانه دارPhosphate buffered saline - فسفات بافر شورpolymerase chain reaction - واکنش زنجیره ای پلیمرازPCR - واکنش زنجیرهٔ پلیمرازprotein kinase A - پروتئین کیناز Amitogen-activated protein kinase - پروتئین کیناز فعال با mitogencellular prion protein - پروتون پریون سلولیCaspase-3 - کاسپاز ۳
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The cellular prion protein (PrPC) is a neuronal-anchored glycoprotein that has been associated with various functions in the CNS such as synaptic plasticity, cognitive processes and neuroprotection. Here we investigated age-related behavioral and neurochemical alterations in wild-type (Prnp+/+), PrPC knockout (Prnp0/0) and the PrPC overexpressing Tg-20 mice. Three- or 11 month-old animals were submitted to a battery of behavioral tasks including open field, activity cages, elevated plus-maze, social recognition and inhibitory avoidance tasks. The 11 month-old Prnp+/+ and Prnp0/0 mice exhibited significant impairments in their locomotor activity and social recognition memory and increased anxiety-related responses. Remarkably, Tg-20 mice did not present these age-related impairments. The i.c.v. infusion of STI1 peptide 230-245, which includes the PrPC binding site, improved the age-related social recognition deficits in Prnp+/+. In comparison with the two other age-matched genotypes, the 11 month-old Tg-20 mice also exhibited reduced activity of seric acetylcholinesterase, increased expression of the protein synaptophysin and decreased caspase-3 positive-cells in the hippocampus. The present findings obtained with genetic and pharmacological approaches provide convincing evidence that PrPC exerts a critical role in the age-related behavioral deficits in mice probably through adaptive mechanisms including apoptotic pathways and synaptic plasticity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 164, Issue 3, 15 December 2009, Pages 896-907
Journal: Neuroscience - Volume 164, Issue 3, 15 December 2009, Pages 896-907
نویسندگان
D. Rial, F.S. Duarte, J.C. Xikota, A.E. Schmitz, A.L. Dafré, C.P. Figueiredo, R. Walz, R.D.S. Prediger,