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成年中枢神经系统中髓鞘形成与GAP - 43表达的相反模式:神经突生长抑制剂作为神经元可塑性的调节因子?

Inverse patterns of myelination and GAP-43 expression in the adult CNS: neurite growth inhibitors as regulators of neuronal plasticity?

作者信息

Kapfhammer J P, Schwab M E

机构信息

Brain Research Institute, University of Zurich, Switzerland.

出版信息

J Comp Neurol. 1994 Feb 8;340(2):194-206. doi: 10.1002/cne.903400206.

DOI:10.1002/cne.903400206
PMID:8201019
Abstract

In the central nervous system (CNS) myelin is present not only in white matter, but also in varying amounts in many gray matter areas. In addition to the function of electrical insulation of axons, myelin and oligodendrocytes contain molecules that are powerful inhibitors of neurite growth. Nevertheless plastic changes involving sprouting of nerve terminals occur in several brain regions of adult animals after partial lesions. In this study we have tried to correlate the plastic potential of CNS regions with the degree of their myelination. The expression of the growth-associated protein GAP-43 was used as an indicator of the potential for plastic changes, and a histological myelin stain was used to assess myelination. We have found that myelination and GAP-43 expression have strikingly inverse expression patterns in the majority of CNS gray matter areas. Densely myelinated regions, that is, most brainstem nuclei, the tegmentum, and the inferior colliculus, are low in GAP-43. In contrast, unmyelinated or lightly myelinated areas, such as the substantia gelatinosa of the spinal cord, the nucleus of the solitary tract, or the septum, express high levels of GAP-43. Areas known to show lesion-induced sprouting are typically high in GAP-43 and only lightly myelinated. During postnatal development the myelination pattern precedes the GAP-43 pattern, a sequence that is consistent with a role of myelin and the associated neurite growth inhibitors in modifying GAP-43 expression. Our results support the hypothesis that myelin-associated neurite growth inhibitors are involved in regulating the stability of neural connections.

摘要

在中枢神经系统(CNS)中,髓磷脂不仅存在于白质中,在许多灰质区域也有不同程度的存在。除了具有轴突电绝缘功能外,髓磷脂和少突胶质细胞还含有对神经突生长有强大抑制作用的分子。然而,成年动物部分损伤后,在几个脑区会发生涉及神经末梢发芽的可塑性变化。在本研究中,我们试图将中枢神经系统区域的可塑性潜力与其髓鞘形成程度联系起来。生长相关蛋白GAP - 43的表达被用作可塑性变化潜力的指标,组织学髓鞘染色用于评估髓鞘形成。我们发现,在大多数中枢神经系统灰质区域,髓鞘形成和GAP - 43表达呈现出明显相反的表达模式。髓鞘密集的区域,即大多数脑干核、被盖和下丘,GAP - 43含量较低。相比之下,无髓鞘或髓鞘较薄的区域,如脊髓胶状质、孤束核或隔区,则表达高水平的GAP - 43。已知会出现损伤诱导发芽的区域通常GAP - 43含量高且髓鞘形成较轻。在出生后发育过程中,髓鞘形成模式先于GAP - 43模式,这一顺序与髓磷脂及相关神经突生长抑制剂在调节GAP - 43表达中的作用一致。我们的结果支持这样一种假说,即髓磷脂相关的神经突生长抑制剂参与调节神经连接的稳定性。

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Inverse patterns of myelination and GAP-43 expression in the adult CNS: neurite growth inhibitors as regulators of neuronal plasticity?成年中枢神经系统中髓鞘形成与GAP - 43表达的相反模式:神经突生长抑制剂作为神经元可塑性的调节因子?
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