کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6018887 | 1186530 | 2012 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Endogenous neurotrophins and plasticity following spinal deafferentation
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
DRIMonoaminergic systemsNT-3DβHCGRPNGFdorsal root ganglion - گانگلیون ریشه پشتیBDNF - BDNF یا فاکتور نورونزایی مشتقشده از مغز Spinal cord injury - آسیب نخاعیtyrosine hydroxylase - تیروزین هیدروکسیلازSprouting - جوانه زدنPain - دردDopamine-beta-hydroxylase - دوپامین بتا هیدروکسیلازrhizotomy - ریزوتومیSERT - سختserotonin transporter - سروتونین حمل کنندهSensory Systems - سیستم های حسیsci - علمیnerve growth factor - فاکتور رشد عصبBrain-derived neurotrophic factor - فاکتور نوروتروفی مشتق شده از مغزMechanosensation - مکانیسمسنجیNeurotrophins - نوروتروفین neurotrophin-3 - نوروتروفین-3calcitonin gene-related peptide - پپتید مرتبط با ژن کلسی تونین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Neurons intrinsic to the spinal cord dorsal horn receive input from various classes of long-distance projection systems. Two of the best known of these are primary afferent and descending monoaminergic axons. Together with intrinsic interneurons, activity in these axonal populations shapes the early part of the sensory experience before it is transmitted to supraspinal structures via ascending projection axons. Injury to dorsal roots, which contain the centrally projecting branches of primary afferent axons, results in their permanent disconnection from the spinal cord, as well as sensory dysfunction such as pain. In animals, experimental dorsal root injuries affecting a small number of roots produce dynamic behavioural changes, providing evidence for the now familiar concept that sensory processing at the level of the spinal cord is not hard-wired. Changes in behaviour following rhizotomy suggest changes in spinal sensory circuitry, and we and others have shown that the density of spinal serotonergic axons as well as processes of inhibitory interneurons increases following rhizotomy. Intact primary afferent axons are less apt to sprout into denervated territory. Recent work from our group has asked (1) what is the stimulus that induces sprouting of serotonergic (and other) axons and (2) what prevents spared primary afferent axons from occupying the territory of those lost to injury. This article will review the evidence that a single factor upregulated by dorsal root injury, brain-derived neurotrophic factor (BDNF), underpins both serotonergic sprouting and a lack of primary afferent plasticity. BDNF also differentially modulates some of the behavioural consequences of dorsal root injury: antagonizing endogenous BDNF improves spontaneous mechanosensory recovery but prevents recovery from rhizotomy-induced hypersensitivity to cold. These findings reinforce the notion that in disease states as complex and variable as spinal cord injury, single pharmacological interventions are unlikely to produce meaningful results. However, understanding the differences in capacity for plasticity among different systems, as well as their triggers, should allow for more patient-tailored therapies.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Neurology - Volume 235, Issue 1, May 2012, Pages 70-77
Journal: Experimental Neurology - Volume 235, Issue 1, May 2012, Pages 70-77
نویسندگان
Matt S. Ramer,