Laurberg S, Zimmer J
J Comp Neurol. 1981 Aug 10;200(3):433-59. doi: 10.1002/cne.902000310.
A lesion-induced formation of an abnormal projection of hippocampal mossy fiber collaterals to the molecular layer of the fascia dentata was studied in rats. Both immature (1--30 days old) and adult rats were subjected to hippocampal and entorhinal lesions which alone or in combination removed one or more of the major afferents to the dentate molecular layer (commissural, associational, and perforant path). Some lesions in addition transected the main part of the mossy fibers en route from the dentate granule cells to the hippocampal pyramidal cells in regio inferior (CA3). The formation of aberrant mossy fiber terminals in fascia dentata (supragranular mossy fibers) was monitored by the histochemical Timm sulphide silver method, but the presence of aberrant terminals was also observed in the electron microscope. Abnormal amounts of supragranular mossy fiber terminals were found following entorhinal lesions of both immature and adult rats, but not following commissural lesions. Even larger amounts of aberrant terminals were, however, found in immature and adult rats subjected to lesions which removed most of the associational hippocampodentate projection by isolating columns of fascia dentata from major parts of the hilus (CA4). Pure transections of the fascia dentata perpendicular to its longitudinal septotemporal axis did not in itself cause aberrant supragranular terminals, although such lesions partially damaged the associational afferents. When the transections were combined with commissural lesions or entorhinal lesions or both, large amounts of supragranular terminals did, however, form at the denervated levels septal to the transection. After comparison of the amounts and distributions of the aberrant terminals found after the different lesions and in transplants of dentate tissue with different amounts of afferent input, we conclude that it is deafferentation of the dentate molecular layer, and not axotomy of the mossy fibers in the hilus of CA3 (pruning), that causes the aberrant growth of mossy fiber collaterals. Moreover, simultaneous removal of more than one afferent system seems to have a potentiating rather than a simple additive effect on the formation of supragranular mossy fibers.
在大鼠中研究了损伤诱导的海马苔藓纤维侧支向齿状回分子层异常投射的形成。未成熟（1 - 30日龄）和成年大鼠均接受海马和内嗅皮层损伤，这些损伤单独或联合去除了齿状回分子层的一种或多种主要传入纤维（连合纤维、联合纤维和穿通通路）。一些损伤还横断了苔藓纤维从齿状颗粒细胞到海马下区（CA3）海马锥体细胞途中的主要部分。通过组织化学硫化银Timm法监测齿状回（颗粒上苔藓纤维）中异常苔藓纤维终末的形成，但在电子显微镜下也观察到了异常终末的存在。未成熟和成年大鼠内嗅皮层损伤后均发现颗粒上苔藓纤维终末数量异常，但连合纤维损伤后未发现。然而，在未成熟和成年大鼠中，通过将齿状回柱与海马体主要部分（CA4）分离而去除大部分联合海马齿状回投射的损伤后，发现了更多的异常终末。垂直于齿状回纵行的前后轴进行单纯横断本身不会导致颗粒上异常终末的形成，尽管这种损伤部分损害了联合传入纤维。然而，当横断与连合纤维损伤或内嗅皮层损伤或两者结合时，在横断水平的隔区失神经支配部位确实形成了大量颗粒上终末。在比较不同损伤后以及不同传入输入量的齿状组织移植中发现的异常终末数量和分布后，我们得出结论，是齿状回分子层的传入纤维切断，而不是CA3海马体门区苔藓纤维的轴突切断（修剪）导致了苔藓纤维侧支的异常生长。此外，同时去除多个传入系统似乎对颗粒上苔藓纤维的形成具有增强作用，而不是简单的累加效应。
