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通过突触靶标切除诱导小鼠[纠正为大鼠]嗅觉神经上皮细胞凋亡。

Induction of apoptosis in mouse [correction of rat] olfactory neuroepithelium by synaptic target ablation.

作者信息

Michel D, Moyse E, Brun G, Jourdan F

机构信息

Laboratoire de Biologie Moléculaire et Cellulaire de l'Ecole Normale Supérieure de Lyon, CNRS UMR 49, France.

出版信息

Neuroreport. 1994 Jun 27;5(11):1329-32.

PMID:7919191
Abstract

The olfactory system provides a useful in vivo model for studying the influence of synaptic targets on the survival of relay neurones. The bipolar sensory neurones located in the olfactory mucosa project synaptically onto the ipsilateral olfactory bulb, and their survival depends on the integrity of this connection. We demonstrate here that the retrograde neuronal degeneration induced by olfactory bulb removal involves apoptosis. As revealed by typical nucleosome-sized fragmentations of the genomic DNA, the apoptosis rate reaches a maximum 32 h after bulbectomy. A transient c-fos mRNA accumulation was detected, peaking 16 h after bulbectomy, suggesting that c-fos is involved in the early steps of programmed cell death.

摘要

嗅觉系统为研究突触靶点对中继神经元存活的影响提供了一个有用的体内模型。位于嗅黏膜的双极感觉神经元通过突触投射到同侧嗅球,它们的存活依赖于这种连接的完整性。我们在此证明,嗅球切除诱导的逆行性神经元变性涉及细胞凋亡。正如基因组DNA典型的核小体大小片段化所揭示的那样,细胞凋亡率在切除嗅球后32小时达到最高。检测到c-fos mRNA短暂积累,在切除嗅球后16小时达到峰值,表明c-fos参与了程序性细胞死亡的早期步骤。

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