کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9416027 | 1292954 | 2005 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Expression of PrPC in the rat brain and characterization of a subset of cortical neurons
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کلمات کلیدی
scrapie prion proteinPNNTSEsPrPscFFICBPPrPcCJDDisorders of the nervous system - اختلالات سیستم عصبیtransmissible spongiform encephalopathy - انسفالوپاتی اسپون های مضرTransmissible spongiform encephalopathies - انسفالوپاتی های اسپگوماییک قابل انتقالFatal familial insomnia - بی خوابی خانوادگی مرگبارCreutzfeldt–Jakob disease - بیماری Creutzfeldt-JakobPerineuronal net - خالص Perineuronalperineuronal nets - شبکه های perineuronalWistar rat - موش ویستارMediodorsal thalamic nucleus - هسته تالامیک MedidorsalParvalbumin - پاروالبومینcalcium-binding protein - پروتئین متصل به کلسیمcalcium-binding proteins - پروتئین های مرتبط با کلسیمPrion protein - پروتئین پریونcellular prion protein - پروتون پریون سلولیCalretinin - کالورتینینcalbindin - کلبیندین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Expression of PrPC in the rat brain and characterization of a subset of cortical neurons Expression of PrPC in the rat brain and characterization of a subset of cortical neurons](/preview/png/9416027.png)
چکیده انگلیسی
The cellular prion protein (PrPC) is a membrane-bound glycoprotein mainly present in the CNS. The scrapie prion protein (PrPSc) is an isoform of PrPC, and it is responsible for transmissible spongiform encephalopathies (TSEs), a group of neurodegenerative diseases affecting both humans and animals. The presence of the cellular form is necessary for the establishment and further evolution of prion diseases. Here, we map the regional distribution of PrPC in the rat brain and study the chemical nature of these immunopositive neurons. Our observations are congruent with retrograde transport of prions, as shown by the ubiquitous distribution of PrPC throughout the rat brain, but especially in the damaged areas that send projections to primarily affected nuclei in fatal familial insomnia. On the other hand, the presence of the cellular isoform in a subset of GABAergic neurons containing calcium-binding proteins suggests that PrPC plays a role in the metabolism of calcium. The lack of immunostaining in neurons ensheathed by perineuronal nets indicates that prions do not directly interact with components of these nets. The destruction of these nets is more likely to be the consequence of a factor needed for prions during the early stages of TSEs. This would cause destruction of these nets and death of the surrounded neurons. Our results support the view that destruction of this extracellular matrix is caused by the pathogenic effect of prions and not a primary event in TSEs.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1056, Issue 1, 14 September 2005, Pages 10-21
Journal: Brain Research - Volume 1056, Issue 1, 14 September 2005, Pages 10-21
نویسندگان
Francisco J. Moleres, José L. Velayos,