DESTRUCTION OF MENINGEAL CELLS OVER THE MEDIAL CEREBRAL HEMISPHERE OF NEWBORN HAMSTERS PREVENTS THE FORMATION OF THE INFRAPYRAMIDAL BLADE OF THE DENTATE GYRUS
DESTRUCTION OF MENINGEAL CELLS OVER THE MEDIAL CEREBRAL HEMISPHERE OF NEWBORN HAMSTERS PREVENTS THE FORMATION OF THE INFRAPYRAMIDAL BLADE OF THE DENTATE GYRUS
复制标题
DOI：
10.1002/cne.903200103
复制
发表时间：
1992-06-01
影响因子：
2.5
通讯作者：
BERRY, M
中科院分区：
文献类型：
--
作者：
HARTMANN, D;SIEVERS, J;BERRY, M
脑膜细胞通过稳定脑顶表面的细胞外基质、组织放射状胶质支架和小脑皮层的层压参与小脑的发育。在本研究中，我们研究了脑膜细胞对齿状回发育的可能影响，其个体发生与小脑有许多相似之处。将25 μ g 6-羟多巴胺（6-OHDA）注入新生小鼠的脑间裂，选择性地破坏脑膜细胞。注射24小时后，大脑内侧半球的脑膜细胞被完全破坏。第30天，齿状回的锥体下叶几乎完全消失，而锥体上叶肥大，其内侧尖端几乎延伸到皮层的内侧表面。为了确定这种发育不良是由脑膜细胞的破坏引起的，另一组仓鼠用去甲肾上腺素（NMN）预处理，它可以抑制脑膜细胞对6-OHDA的神经元外摄取。在6-OHDA加NMN治疗后的第30天，脑膜细胞未受影响，齿状回形态正常。当脑膜细胞在发育后期（出生后1-5天）被破坏时，齿状回的改变只能诱导到出生后第4天；此后，6-OHDA治疗使其保持不变。这表明脑膜细胞影响的关键时期与脑膜下齿状基质的存在时期相吻合。对发育缺陷的时间过程进行分析，发现在头5天，1)大脑内侧半球上的脑膜细胞被破坏和移除，2)齿状体和间脑上的脑基底膜变薄破裂，邻近脑部分局部融合，3)脑下齿状体基质的许多细胞从其下表面位置消失。4)门部和锥体上叶的亚颗粒区“未成熟”细胞数量增加；5)锥体上叶明显拉长和增厚，锥体下叶未形成。超过5天后，未与间脑融合的齿状体基底面部分被脑膜细胞重新填充。脑膜细胞的重新出现伴随着1)基底膜的正常形态的恢复，2)枕表面下神经元和胶质细胞的重新出现，以及3)锥体下叶碎片的形成，这些碎片后来发展为正常的层压。这些发现表明脑膜细胞至少参与了齿状回锥体下叶的发育。这种影响的机制目前仍是推测性的，但可能包括：1)脑膜细胞参与脑膜表面细胞外基质的重塑；2)脑膜下齿状突基质和齿状回锥体下叶中神经元和胶质细胞的空间分布和组织的调节。
Meningeal cells participate in the development of the cerebellum both by stabilizing the extracellular matrix of the pial surface and by organizing the radial glial scaffold and the lamination of the cerebellar cortex. In the present study we investigated possible influences of meningeal cells on the development of the dentate gyrus, whose ontogenesis has many similarities to that of the cerebellum. Meningeal cells were selectively destroyed by injecting newborn hamsters with 25-mu-g 6-hydroxydopamine (6-OHDA) into the interhemispheric fissure. Twenty-four hours postinjection (p.i.) the meningeal cells over the medial cerebral hemispheres were completely destroyed. Thirty days p.i. the infrapyramidal blade of the dentate gyrus was almost completely missing, while the suprapyramidal blade was hypertrophied, extending with its medial tip almost up to the medial surface of the cortex. In order to ascertain that this maldevelopment was caused by the destruction of meningeal cells, another group of hamsters was pretreated with normetanephrine (NMN) which inhibits the extraneuronal uptake of 6-OHDA into meningeal cells. In this group the meningeal cells were unaffected by the treatment, and the morphology of the dentate gyrus was normal 30 days p.i. of 6-OHDA plus NMN.When the meningeal cells were destroyed in later stages of development (postnatal days 1-5), alterations of the dentate gyrus could be induced only up to the fourth postnatal day; thereafter, 6-OHDA treatment left it unchanged. This indicates a critical period of meningeal cell influence that coincides with the period of existence of the subpial dentate matrix.Analysis of the time course of the defective development revealed that in the first 5 days p.i. 1) meningeal cells over the medial cerebral hemisphere were destroyed and removed, 2) the pial basement membrane over both the dentate anlage and the diencephalon thinned and ruptured, and the adjacent brain parts fused focally, 3) many cells of the subpial dentate matrix disappeared from their subsurface position, 4) the number of "immature" cells increased in the hilus and the subgranular zone of the suprapyramidal blade, 5) the suprapyramidal blade elongated and thickened considerably, while the infrapyramidal blade did not form. Beyond 5 days p.i. those parts of the pial surface of the dentate anlage that had not fused with the diencephalon were repopulated with meningeal cells. This reappearance of meningeal cells was accompanied by 1) the restitution of the normal morphology of the basement membrane, 2) the reappearance of neuronal and glial cells below the pial surface, and 3) the formation of fragments of the infrapyramidal blade which later developed a normal appearing lamination.These findings show that meningeal cells are involved in the development of at least the infrapyramidal blade of the dentate gyrus. The mechanisms of this influence remain speculative at present, but probably include 1) participation of the meningeal cells in the remodelling of the extracellular matrix of the pial surface, and 2) the regulation of the spatial distribution and organization of the neuronal and glial cells in the subpial dentate matrix and the infrapyramidal blade of the dentate gyrus.