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大鼠齿状回兴奋性内嗅输入损伤后抑制性连合纤维萌出的形态学证据。

Morphological evidence for the sprouting of inhibitory commissural fibers in response to the lesion of the excitatory entorhinal input to the rat dentate gyrus.

作者信息

Deller T, Frotscher M, Nitsch R

机构信息

Institute of Anatomy, University of Freiburg, Germany.

出版信息

J Neurosci. 1995 Oct;15(10):6868-78. doi: 10.1523/JNEUROSCI.15-10-06868.1995.

DOI:10.1523/JNEUROSCI.15-10-06868.1995
PMID:7472444
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6578021/
Abstract

Recently a commissural fiber projection that terminates in the outer molecular layer of the fascia dentata was described in normal rats (Deller et al., 1995). In the present article, Phaseolus vulgaris leucoagglutinin (PHAL) tracing was used to analyze the contribution of this previously unknown projection to the commissural sprouting response after entorhinal cortex lesion. Rats 4-8 weeks after unilateral entorhinal lesion received a single PHAL deposit into the hilus of the fascia dentata contralateral to the lesion side. Unlesioned control animals received a similar PHAL deposit. The degree of axonal arborization and the bouton density per axon length were determined for individual PHAL-labeled commissural axons to the outer molecular layer of the dentate gyrus. A significant increase in both parameters was observed in the lesioned group. The PHAL-labeled commissural fibers established symmetric synapses in the denervated outer molecular layer. Postembedding immunocytochemistry indicated that some of these sprouting commissural fibers are GABAergic. Our findings provide morphological evidence for lamina-specific sprouting of an inhibitory commissural projection that normally terminates in the outer molecular layer. This suggests that inhibitory fibers participate in the replacement of the excitatory perforant pathway after entorhinal lesion.

摘要

最近,在正常大鼠中发现了一种终止于齿状回外分子层的连合纤维投射(Deller等人,1995年)。在本文中,使用菜豆白细胞凝集素(PHAL)追踪技术来分析这种先前未知的投射对内嗅皮层损伤后连合芽生反应的贡献。单侧内嗅损伤4-8周后的大鼠在损伤侧对侧的齿状回门区接受单次PHAL注射。未损伤的对照动物接受类似的PHAL注射。对于单个PHAL标记的投射到齿状回外分子层的连合轴突,测定其轴突分支程度和每轴突长度的终扣密度。在损伤组中观察到这两个参数均显著增加。PHAL标记的连合纤维在去神经支配的外分子层中形成对称突触。包埋后免疫细胞化学表明,这些芽生的连合纤维中有一些是γ-氨基丁酸能的。我们的研究结果为通常终止于外分子层的抑制性连合投射的层特异性芽生提供了形态学证据。这表明抑制性纤维参与了内嗅损伤后兴奋性穿通通路的替代。