Neuroplasticity in the olfactory system: Differential effects of central and peripheral lesions of the primary olfactory pathway on the expression of B‐50/GAP43 and the olfactory marker protein
Neuroplasticity in the olfactory system: Differential effects of central and peripheral lesions of the primary olfactory pathway on the expression of B‐50/GAP43 and the olfactory marker protein
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嗅觉系统的神经可塑性：初级嗅觉通路中枢和外周病变对 B-50/GAP43 和嗅觉标记蛋白表达的差异影响
DOI：
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发表时间：
1990
影响因子：
4.2
通讯作者：
F. Margolis
中科院分区：
文献类型：
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作者：
J. Verhaagen;A. Oestreicher;M. Grillo;Y. Khew;W. Gispen;F. Margolis
用mRNA探针和B‐50/GAP43和嗅觉标记蛋白（OMP）抗体研究嗅球切除或外周神经分化后嗅神经上皮的再生。嗅觉上皮的再生可分为两个阶段。第一阶段发生在Triton X‐100 （TX‐100）对嗅上皮进行外周神经分化后或球根切除术后，其特征是形成大量未成熟的嗅觉受体神经元。这些新形成的神经元表达B‐50/GAP43，这是一种与神经元生长和可塑性相关的磷酸化蛋白。在再生过程的第二阶段，新形成的嗅觉神经元成熟，证明了它们的B‐50/GAP43表达减少和OMP表达增加。这一阶段只有在发育中的神经元能够接触到目标嗅球时才会表现出来。表达OMP‐的神经元的完整补体的形成只发生在外周损伤与TX‐100。相比之下，在球部切除后，重建的嗅上皮缺乏其正常的靶点，并且其从神经损伤中恢复的能力受到损害，这可以从损伤后3个月存在大量表达B‐50/GAP43‐的神经元以及无法建立完整的表达OMP‐的神经元中得到证明。这些结果表明，嗅觉上皮能够独立于其目标嗅球的存在而替换其感觉神经元。然而，在外周病变（TX - 100）或嗅球切除术后很长一段时间内，B‐50/GAP43和OMP的不同表达模式表明，嗅球对重建嗅神经上皮的神经元成熟有深远的影响。
The regeneration of the olfactory neuroepithelium following olfactory bulbectomy or peripheral deafferentation was studied with mRNA probes and antibodies for B‐50/GAP43 and for olfactory marker protein (OMP). Two stages in the regeneration of the olfactory epithelium could be discerned with these reagents. The first stage occurs following either peripheral deafferentation of the olfactory epithelium with Triton X‐100 (TX‐100) or after bulbectomy and is characterized by the formation of a large population of immature olfactory receptor neurons. These newly formed neurons express B‐50/GAP43, a phosphoprotein related to neuronal growth and plasticity. During the second stage of the regeneration process the newly formed olfactory neurons mature, as evidenced by a decrease in their expression of B‐50/GAP43 and an increase in the expression of OMP. This stage is only manifested if the developing neurons have access to the target olfactory bulb. Formation of a full complement of OMP‐expressing neurons occurs only after peripheral lesion with TX‐100. In contrast, following bulbectomy the reconstituted olfactory epithelium lacks its normal target and is compromised in its ability to recover from nerve damage, as evidenced by the presence of a large number of B‐50/GAP43‐expressing neurons up to 3 months after the lesion and its failure to establish a full complement of OMP‐expressing neurons. These results demonstrate that the olfactory epithelium is capable of replacing its sensory neurons independently of the presence of its target, the olfactory bulb. However, the differential patterns of expression of B‐50/GAP43 and OMP at long times after peripheral lesion with TX‐100 or bulbectomy illustrate the profound effect the olfactory bulb has on neuronal maturation in reconstituted olfactory neuroepithelium.