Immunocytochemical heterogeneity of somatostatin‐expressing GABAergic interneurons in layers II and III of the mouse cingulate cortex: A combined immunofluorescence/design‐based stereologic study

帕尔瓦布明 加巴能 中间神经元 钙黄绿素 生物 神经科学 扣带皮质 神经肽 皮质(解剖学) 人口 生长抑素 扣带回前部 钙粘蛋白 抑制性突触后电位 中枢神经系统 免疫组织化学 受体 遗传学 医学 免疫学 认知 环境卫生
作者
Therese Riedemann,Christoph Schmitz,Bernd Sutor
出处
期刊:Journal of comparative neurology [Wiley]
卷期号:524 (11): 2281-2299 被引量:20
标识
DOI:10.1002/cne.23948
摘要

ABSTRACT Many neurological diseases including major depression and schizophrenia manifest as dysfunction of the GABAergic system within the cingulate cortex. However, relatively little is known about the properties of GABAergic interneurons in the cingulate cortex. Therefore, we investigated the neurochemical properties of GABAergic interneurons in the cingulate cortex of FVB‐Tg(GadGFP)45704Swn/J mice expressing green fluorescent protein (GFP) in a subset of GABAergic interneurons (GFP‐expressing inhibitory interneurons [GINs]) by means of immunocytochemical and design‐based stereologic techniques. We found that GINs represent around 12% of all GABAergic interneurons in the cingulate cortex. In contrast to other neocortical areas, GINs were only found in cortical layers II and III. More than 98% of GINs coexpressed the neuropeptide somatostatin (SOM), but only 50% of all SOM + neurons were GINs. By analyzing the expression of calretinin (CR), calbindin (CB), parvalbumin, and various neuropeptides, we identified several distinct GIN subgroups. In particular, we observed coexpression of SOM with CR and CB. In addition, we found neuropeptide Y expression almost exclusively in those GINs that coexpressed SOM and CR. Thus, with respect to the expression of calcium‐binding proteins and neuropeptides, GINs are surprisingly heterogeneous in the mouse cingulate cortex, and the minority of GINs express only one marker protein or peptide. Furthermore, our observation of overlap between the SOM + and CR + interneuron population was in contrast to earlier findings of non‐overlapping SOM + and CR + interneuron populations in the human cortex. This might indicate that findings in mouse models of neuropsychiatric diseases may not be directly transferred to human patients. J. Comp. Neurol. 524:2281–2299, 2016. © 2015 Wiley Periodicals, Inc.
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