Steward O, Vinsant S L
Brain Res. 1978 May 26;147(2):223-43. doi: 10.1016/0006-8993(78)90837-5.
Following unilateral destruction of the entorhinal cortical region of the adult rat, the denervated granule cells of the dentate gyrus are reinnervated as a result of the proliferation of a pathway from the surviving contralateral entorhinal area. The present study investigates the cells of origin of this lesion-induced pathway. Following HRP injections into the reinnervated dentate gyrus, heavily labeled cells were evident in layers II and III of the contralateral entorhinal area, in marked contrast to the pattern of labeling in normal animals, where labeled cells are restricted almost entirely to layer III. The atypically labeled cells in the operated animals were found predominantly in the dorsal half of the entorhinal area, and were concentrated in the medial most portion of layer II. These atypically labeled cells in layer II of the operated animals were an average of 16% larger than their unlabeled neighbors in the same lamina. This was not related to the loading with HRP, however, since in normal animals, cells in layer II which are labeled with HRP were no different in size than unlabeled cells. The atypically labeled cells in layer II of operated animals could also be identified at the electron microscopic level, and could be distinguished from the cells in layer III which normally project to regio superior of the contralateral hippocampal formation. While labeled cells were evident in layers II and III following injections into the reinnervated dentate gyrus, no labeled cells were found in the presubiculum or parasubiculum. In combination, these results suggest (1) the pathway which reinnervates the dentate gyrus from the contralateral entorhinal area originates predominantly, if not exclusively, from the cells in layer II, (2) these cells in layer II have the same preferential distribution within the entorhinal area as the rare lightly labeled cells which can be found contralateral to an injection in normal animals and (3) cells which participate in the reinnervation are larger than their unlabeled neighbors which presumably do not give rise to fibers which reinnervate the contralateral dentate gyrus. Since the cells in layer II which sprout following lesions can be identified at both the light and elctron microscopic level, a potentially valuable model system is available in which to analyze cellular changes during sprouting.
成年大鼠内嗅皮质区域单侧损毁后，齿状回去神经支配的颗粒细胞会因来自对侧存活内嗅区域的一条通路的增殖而重新获得神经支配。本研究调查了这条损伤诱导通路的起源细胞。将辣根过氧化物酶（HRP）注入重新获得神经支配的齿状回后，对侧内嗅区域的II层和III层出现了大量标记细胞，这与正常动物的标记模式形成显著对比，在正常动物中，标记细胞几乎完全局限于III层。手术动物中异常标记的细胞主要位于内嗅区域的背侧半部，并集中在II层最内侧部分。手术动物II层中这些异常标记的细胞比同一层中未标记的相邻细胞平均大16%。然而，这与HRP的负载无关，因为在正常动物中，用HRP标记的II层细胞大小与未标记细胞没有差异。手术动物II层中异常标记的细胞在电子显微镜水平也能被识别，并且可以与通常投射到对侧海马结构上区的III层细胞区分开来。虽然向重新获得神经支配的齿状回注射后II层和III层出现了标记细胞，但在海马旁回或副海马旁回未发现标记细胞。综合这些结果表明：（1）从对侧内嗅区域重新支配齿状回的通路如果不是完全起源于II层细胞，也主要起源于这些细胞；（2）II层中的这些细胞在内嗅区域内的优先分布与正常动物中与注射对侧罕见的轻度标记细胞相同；（3）参与重新神经支配的细胞比其未标记的相邻细胞大，这些未标记的相邻细胞大概不会产生重新支配对侧齿状回的纤维。由于损伤后II层中发芽的细胞在光学显微镜和电子显微镜水平都能被识别，因此有一个潜在有价值的模型系统可用于分析发芽过程中的细胞变化。
