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体外红藻氨酸对大型、SMI-32(+)脊髓神经元的损伤是钙离子依赖性的。

In vitro kainate injury to large, SMI-32(+) spinal neurons is Ca2+ dependent.

作者信息

Carriedo S G, Yin H Z, Lamberta R, Weiss J H

机构信息

Department of Neurology, University of California Irvine 92717-4290, USA.

出版信息

Neuroreport. 1995 Apr 19;6(6):945-8. doi: 10.1097/00001756-199504190-00030.

Abstract

The non-phosphorylated neurofilament marker, SMI-32, identifies ventral horn motor neurons in spinal cord slice. We show here that SMI-32 marks a subset of spinal cord neurons in culture. Many of these neurons ('large SMI-32(+) neurons') have morphological characteristics of identified motor neurons in vitro: large cell body size (> 20 microns), extensive neuritic arborization and, generally, one particularly long process. These neurons are preferentially injured by brief (40 min) kainate exposures, but not by NMDA exposures. This rapidly triggered damage to large SMI-32(+) neurons is Ca2+ dependent. In addition, most of the SMI-32(+) neurons exhibit kainate-stimulated Co2+ uptake, a histochemical technique which marks neurons possessing Ca(2+)-permeable AMPA/kainate receptor-gated channels. The unusual vulnerability of large SMI-32(+) spinal neurons to kainate toxicity may result from rapid Ca2+ entry through Ca(2+)-permeable AMPA/kainate channels.

摘要

非磷酸化神经丝标志物SMI-32可识别脊髓切片中的腹角运动神经元。我们在此表明,SMI-32标记了培养中的一部分脊髓神经元。这些神经元中的许多(“大型SMI-32(+)神经元”)在体外具有已识别运动神经元的形态特征:细胞体大(>20微米)、广泛的神经分支,并且通常有一个特别长的突起。这些神经元优先受到短暂(40分钟)的海藻酸暴露损伤,但不受NMDA暴露损伤。这种对大型SMI-32(+)神经元的快速触发损伤是钙依赖性的。此外,大多数SMI-32(+)神经元表现出海藻酸刺激的钴摄取,这是一种组织化学技术,可标记具有钙通透性AMPA/海藻酸受体门控通道的神经元。大型SMI-32(+)脊髓神经元对海藻酸毒性的异常易感性可能是由于通过钙通透性AMPA/海藻酸通道的快速钙内流所致。

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