Distribution of calbindin D-28k in the entorhinal, perirhinal, and parahippocampal cortices of the macaque monkey.

Distribution of calbindin D-28k in the entorhinal, perirhinal, and parahippocampal cortices of the macaque monkey.
复制标题

钙结合蛋白 D-28k 在猕猴内嗅、鼻周和海马旁皮质中的分布。

DOI:
10.1002/cne.10370
复制
发表时间:
2002
期刊:
The Journal of comparative neurology.
影响因子:
--
通讯作者:
Porteros,Angel
Porteros,Angel
中科院分区:
--
文献类型:
--
作者:
Suzuki,WendyA;Porteros,Angel

文献摘要

相似文献

We examined the distribution of calbindin D‐28k–immunoreactive (CB‐IR) neurons, fibers, and neuropil in the entorhinal (area 28), perirhinal (areas 35 and 36), and parahippocampal (areas TH and TF) cortices in the macaque monkey. Two main findings are reported. First, except for CB‐IR neurogliaform cells that are only observed in the parahippocampal cortex, the morphology of CB‐stained pyramidal and nonpyramidal cells were similar across the three cortical areas examined. Second, we find that the topography of CB staining differed between the three areas. The entorhinal cortex exhibits the most striking gradient of CB staining such that the most anterior and medial portions are most strongly labeled, whereas posterior and lateral areas exhibit only weak labeling. The labeling throughout the perirhinal and parahippocampal cortices is more homogeneous. Area 35 contains only lightly stained neuropil and few CB‐IR cells. Area 36 and areas TH and TF of the parahippocampal cortex contain a moderate to high density of CB‐IR cells and fibers throughout their full rostrocaudal extents, although each area exhibits unique laminar patterns of staining. In all areas examined, the highest density of CB‐positive cells and fibers is observed in superficial layers with lower densities of CB‐positive cells and fibers present in deep layers. These findings, taken together with our current understanding of the connections of these areas may have implications for understanding the circuit properties of the entorhinal, perirhinal, and parahippocampal cortices areas in both normal and disease states. J. Comp. Neurol. 451:392–412, 2002. © 2002 Wiley‐Liss, Inc.