Polysialic acid-induced plasticity reduces neuropathic insult to the central nervous system
Polysialic acid-induced plasticity reduces neuropathic insult to the central nervous system
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DOI：
10.1073/pnas.0504718102
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发表时间：
2005-08-09
影响因子：
11.1
通讯作者：
Rutishauser, U
中科院分区：
文献类型：
--
作者：
El Maarouf, A;Kolesnikov, Y;Rutishauser, U
在神经病理性疼痛的慢性条件下，伤害性C终末从脊髓板层11的靶区丢失，导致热痛敏减少。脊髓的这一区域表达高水平的聚唾液酸(PSA)，这是一种已知的细胞表面碳水化合物，可以削弱细胞与细胞之间的相互作用，促进可塑性。实验性地将PSA从脊髓中移除会加剧痛觉过敏并导致C终末滞留，但对触觉Aβ纤维的可塑性和痛觉异常没有影响。我们认为，PSA在这个应激通路中继点的表达可能有助于保护中枢回路免受慢性感觉超负荷的影响。
Under chronic conditions of neuropathic pain, nociceptive C terminals are lost from their target region in spinal lamina 11, leading to reduced thermal hyperalgesia. This region of the spinal cord expresses high levels of polysialic acid (PSA), a cell surface carbohydrate known to weaken cell-cell interactions and promote plasticity. Experimental removal of PSA from the spinal cord exacerbates hyperalgesia and results in retention of C terminals, whereas it has no effect on plasticity of touch A beta fibers and allodynia. We propose that expression of PSA at this stress pathway relay point could serve to protect central circuitry from chronic sensory overload.