NMDA receptor expression in the mouse cerebellar cortex.

NMDA receptor expression in the mouse cerebellar cortex.
复制标题

小鼠小脑皮质中 NMDA 受体的表达。

DOI:
10.1002/syn.890200310
复制
发表时间:
1995
期刊:
Synapse (New York, N.Y.)
影响因子:
--
通讯作者:
Morest,DK
Morest,DK
中科院分区:
--
文献类型:
--
作者:
Bilak,SR;Bilak,MM;Morest,DK

文献摘要

相似文献

采用免疫组织化学和原位杂交对小鼠小脑皮质N-甲基-D-天冬氨酸受体亚单位1(NMDAR 1)的分布进行了详细的光镜研究。使用单克隆抗体,浦肯野细胞体的标记从强烈到阴性变化,而重树突染色仅限于近端树突(与大鼠不同,其也具有重染色的远端树突)。在颗粒层中,高尔基体II细胞的细胞体和树突状轴仅中度染色,但非常强烈的标记与颗粒细胞体,并与他们的树突和树突状末梢在肾小球。苔藓纤维和攀缘纤维呈阴性。原位杂交与cRNA探针显示NMDAR 1 mRNA的水平和空间分布与免疫标记模式一致,在该信号是最强的颗粒和浦肯野细胞层和相对较低或不存在的分子层和白色物质。这一发现与NMDAR 1可能特别集中在苔藓纤维和攀缘纤维的突触靶位点的假设是一致的。在小鼠中,与浦肯野细胞多刺小枝相关的平行纤维部位的NMDAR 1在其表达水平或分子构型上可能与大鼠不同。© 1995 Wiley利斯公司
A detailed, light microscopic study on the distribution of the N‐methyl‐D‐aspartate receptor subunit 1(NMDAR1) was carried out with immunohistochemistry and in situ hybridization on the cerebellar cortex of the mouse. With a monoclonal antibody, labeling of Purkinje cell bodies varied from intense to negative, while heavy dendritic staining was limited to the proximal dendrites (unlike the rat, which also had heavily stained distal dendrites). In the granular layer, the cell bodies and the dendritic shafts of Golgi II cells were only moderately stained, but very intense labeling was associated with granule cell bodies, and with their dendrites and dendritic endings in the glomeruli. The mossy and climbing fibers were negative. In situ hybridization with a cRNA probe showed levels and spatial distributions of NMDAR1 mRNA consistent with the immunolabeling pattern, in that signals were strongest in the granular and Purkinje cell layers and relatively low or absent in the molecular layer and white matter. The findings are consistent with the hypothesis that NMDAR1 may be especially well concentrated at the synaptic target sites of the mossy and climbing fibers. In the mouse, NMDAR1 at the parallel fiber sites associated with Purkinje cell spiny branchlets may differ from the rat in its level of expression or in its molecular configuration. © 1995 Wiley‐Liss, Inc.