Cortical sensory map rearrangement after spinal cord injury:: fMRI responses linked to Nogo signalling
Cortical sensory map rearrangement after spinal cord injury:: fMRI responses linked to Nogo signalling
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DOI：
10.1093/brain/awm237
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发表时间：
2007-11-01
期刊：
影响因子：
14.5
通讯作者：
Olson, Lars
中科院分区：
文献类型：
--
作者：
Endo, Toshiki;Spenger, Christian;Olson, Lars
皮质感觉图可以在成人大脑中以依赖于经验的方式进行重组。我们使用功能性磁共振成像（fMRI）监测中胸脊髓完全横断的大鼠感觉传入神经阻滞后的体感皮质重组。早在受伤后 3 天，就观察到对未受前肢刺激的皮质表征扩大并侵入初级体感皮层中邻近的感觉剥夺后肢区域。功能性 MRI 还显示出长期皮质可塑性，并伴随着丘脑激活的增加。为了支持脊髓损伤后皮质神经元回路的改变可能是功能磁共振成像变化的基础这一观点，我们利用原位杂交量化了与皮质可塑性相关的几个基因的转录活性，包括Nogo受体（NgR）、其共同受体LINGO-1和脑源性神经营养因子（BDNF）。我们证明，从受伤后 1 天起，NgR 和 LINGO-1 在缺乏感觉输入的皮质区域和邻近皮质中特别下调，而 BDNF 则上调。我们的结果表明，皮质神经元通过降低感觉剥夺区域和解剖学上相邻的非剥夺区域中编码 Nogo 受体成分的基因的转录活性来对感觉剥夺做出反应。与 BDNF 上调相结合，这些变化可能会导致神经毡的结构发生变化。因此，我们的观察表明 Nogo 信号参与了体感系统中皮质活动依赖性可塑性。在脊髓损伤中，如图所示的皮质重组可能会成为一种劣势，就像弱视或幻觉的情况一样。一旦被剥夺的后肢皮质区域被重新分配给前肢使用，在脊髓水平修复感觉通路的成功策略可能不会导致皮质连接的正确重建。在这种情况下，控制皮质可塑性的方法（可能通过针对 Nogo 信号传导）可能会有所帮助。
Cortical sensory maps can reorganize in the adult brain in an experience-dependent manner. We monitored somatosensory cortical reorganization after sensory deafferentation using functional magnetic resonance imaging (fMRI) in rats subjected to complete transection of the mid-thoracic spinal cord. Cortical representation in response to spared forelimb stimulation was observed to enlarge and invade adjacent sensory-deprived hind limb territory in the primary somatosensory cortex as early as 3 days after injury. Functional MRI also demonstrated long-term cortical plasticity accompanied by increased thalamic activation. To support the notion that alterations of cortical neuronal circuitry after spinal cord injury may underlie the fMRI changes, we quantified transcriptional activities of several genes related to cortical plasticity including the Nogo receptor (NgR), its co-receptor LINGO-1 and brain derived neurotrophic factor (BDNF), using in situ hybridization. We demonstrate that NgR and LINGO-1 are down-regulated specifically in cortical areas deprived of sensory input and in adjacent cortex from 1 day after injury, while BDNF is up-regulated. Our results demonstrate that cortical neurons react to sensory deprivation by decreasing transcriptional activities of genes encoding the Nogo receptor components in the sensory deprived and the anatomically adjacent non-deprived area. Combined with the BDNF up-regulation, these changes presumably allow structural changes in the neuropil. Our observations therefore suggest an involvement of Nogo signalling in cortical activity-dependent plasticity in the somatosensory system. In spinal cord injury, cortical reorganization as shown here can become a disadvantage, much like the situation in amblyopia or phantom sensation. Successful strategies to repair sensory pathways at the spinal cord level may not lead to proper reestablishment of cortical connections, once deprived hind limb cortical areas have been reallocated to forelimb use. In such situations, methods to control cortical plasticity, possibly by targeting Nogo signalling, may become helpful.