Expression profile of receptors for myelin-associated inhibitors of axonal regeneration in the intact and injured mouse central nervous system
Expression profile of receptors for myelin-associated inhibitors of axonal regeneration in the intact and injured mouse central nervous system
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DOI：
10.1016/j.mcn.2006.12.004
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发表时间：
2007-04-01
影响因子：
3.5
通讯作者：
Lacroix, Steve
中科院分区：
文献类型：
--
作者：
Barrette, Benoit;Vallieres, Nicolas;Lacroix, Steve
尽管CNS神经元在损伤后具有再生其轴突的潜力，但携带轴突生长抑制剂的髓鞘碎片迅速诱导生长锥塌陷。这些抑制剂的受体（NgR 1，NgR 2）和辅助受体（LINGO-1，p75（NTR），TROY）已被表征，并部分确定了转导途径。然而，很少有人知道这些受体的表达在完整的和受损的脊髓上投射神经元。利用原位杂交，免疫组织化学和神经元束示踪，我们发现，NgR 1，NgR 2和LINGO-1强烈表达在几个神经元群体的成年小鼠大脑投射到脊髓，包括神经元投射通过皮质脊髓，红核脊髓，caerulospinal，网状脊髓，中缝脊髓和vestibulospinal束。正如预期的那样，p75（NTR）表达仅限于脑干的神经元下行通路。大多数脑区和所有神经元投射系统都没有TROY，这表明存在额外的信号转导辅助受体。定性和定量分析表明，这些受体的大脑表达没有受到严重的T10脊髓挫伤。(c)2006年爱思唯尔公司All rights reserved.
Although CNS neurons have the potential to regenerate their axons after injury, myelin debris carrying axon growth inhibitors rapidly induce growth cone collapse. Receptors (NgR1, NgR2) and coreceptors (LINGO-1, p75(NTR), TROY) for these inhibitors have been characterized and transduction pathways partially identified. However, little is known about the expression of these receptors in intact and lesioned supraspinal projection neurons. Using in situ hybridization, immunohistochemistry and neuronal tract-tracing, we found that NgR1, NgR2 and LINGO-1 are strongly expressed in several neuronal populations of the adult mouse brain projecting to the spinal cord, including neurons projecting through the corticospinal, rubrospinal, caerulospinal, reticulospinal, raphespinal and vestibulospinal tracts. As expected, p75(NTR) expression was restricted to neuronal descending pathways from the brainstem. TROY was absent from most brain regions and from all neuronal projection systems, suggesting that additional signal-transducing coreceptors exist. Qualitative and quantitative analyses revealed that brain expression for these receptors was not affected by a severe T10 spinal cord contusion. (c) 2006 Elsevier Inc. All rights reserved.