کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6273924 | 1614815 | 2014 | 15 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Effects of sustained proNGF blockade on attentional capacities in aged rats with compromised cholinergic system
ترجمه فارسی عنوان
اثرات انسداد پروندۀ پروژکتیو پایدار بر ظرفیت های اطمینان در موش های سالم با سیستم کولینرژیک آسیب پذیر
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کلمات کلیدی
PFCPFANGFSATTBSITIGFPNBMAAVHEPESLSDTBSTtrkAproNGFdSATCHTPBSDABtropomyosin-related kinase A3-3′-diaminobenzidine2-[4-(2-hydroxyethyl)piperazin-1-yl]ethanesulfonic acid - 2- [4- (2-hydroxyethyl) piperazin-1-yl] ethanesulfonic acidAscorbic acid - آسکوربیک اسیدACh - آهAcetylcholine - استیل کولینAlzheimer’s disease - بیماری آلزایمرanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of varianceTris-buffered saline - تریس بافر شورAttention - توجهLOD یا Limit of detection - حد تشخیصleast significant difference - حداقل تفاوت قابل توجهیstandard error of the mean - خطای استاندارد میانگینDopamine - دوپامینAging - سالخوردگیintertrial interval - فاصله بین فضاییnerve growth factor - فاکتور رشد عصبprefrontal cortex - قشر prefrontalsubstantia innominata - ماده تعیین شدهlimit of detection - محدودیت تشخیصPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریSEM - مدل معادلات ساختاری / میکروسکوپ الکترونی روبشیnucleus basalis of Meynert - هسته پایه Meynertadeno-associated viral - ویروسی مرتبط با آدنوparaformaldehyde - پارافرمالدهیدgreen fluorescent protein - پروتئین فلورسنت سبزbasal forebrain - پیشانی پایهChAT - چتcholine acetyltransferase - کولین استیل ترانسفرازcholine transporter - کولین حمل کننده
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
چکیده انگلیسی
Disruption in nerve growth factor (NGF) signaling via tropomyosin-related kinase A (trkA) receptors compromises the integrity of the basal forebrain (BF) cholinergic system, yielding cognitive, specifically attentional, impairments in Alzheimer's disease (AD). Although normal aging is considered a risk factor for AD, the mechanisms underlying the selective vulnerability of the aging cholinergic system to trkA disruption is not clear. The levels of proNGF, a proneurotrophin that possesses higher affinity for p75 receptors, increase in aging. The present study was designed to test the hypothesis that cholinergic and attentional dysfunction in aged rats with reduced BF trkA receptors occurs due to the overactivation of endogenous proNGF signaling. We employed a viral vector that produced trkA shRNA to suppress trkA receptors in the corticopetal cholinergic neurons of aged rats. BF trkA suppression impaired animals' performance on signal trials in both the sustained attention task (SAT) and the cognitively taxing distractor version of SAT (dSAT) and these deficits were normalized by chronic intracerebroventricular administration of proNGF antibody. Moreover, depolarization-evoked acetylcholine (ACh) release and the density of cortical cholinergic fibers were partially restored in these animals. However, SAT/dSAT scores reflecting overall performance did not improve following proNGF blockade in trkA knockdown rats due to impaired performance in non-signal trials. Sustained proNGF blockade alone did not alter baseline attentional performance but produced moderate impairments during challenging conditions. Collectively, our findings indicate that barring proNGF-p75 signaling may exert some beneficial effects on attentional capacities specifically when BF trkA signaling is abrogated. However, endogenous proNGF may also possess neurotrophic effects and blockade of this proneurotrophin may not completely ameliorate attentional impairments in AD and potentially hinder performance during periods of high cognitive load in normal aging.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 261, 7 March 2014, Pages 118-132
Journal: Neuroscience - Volume 261, 7 March 2014, Pages 118-132
نویسندگان
B. Yegla, V. Parikh,