Reactive oxygen species and nitric oxide mediate plasticity of neuronal calcium signaling

被引：86
作者：
Yermolaieva, O
Brot, N
Weissbach, H
Heinemann, SH
Hoshi, T
机构：
[1] Univ Iowa, Dept Physiol & Biophys, Iowa City, IA 52242 USA
[2] Cornell Univ, Hosp Special Surg, Med Ctr, New York, NY 10021 USA
[3] Florida Atlantic Univ, Dept Biol Sci, Boca Raton, FL 33431 USA
[4] Univ Jena, Arbeitsgruppe Mol & Zellulare Biophys Klinikum, D-07747 Jena, Germany
来源：
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2000年 / 97卷 / 01期
关键词：
D O I：
10.1073/pnas.97.1.448
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
Reactive oxygen species (ROS) and nitric oxide (NO) are important participants in signal transduction that could provide the cellular basis for activity-dependent regulation of neuronal excitability. In young rat cortical brain slices and undifferentiated PC12 cells, paired application of depolarization/agonist stimulation and oxidation induces long-lasting potentiation of subsequent Ca2+ signaling that is reversed by hypoxia. This potentiation critically depends on NO production and involves cellular ROS utilization. The ability to develop the Ca2+ signal potentiation is regulated by the developmental stage of nerve tissue, decreasing markedly in adult rat cortical neurons and differentiated PC12 cells.
引用
收藏
页码：448 / 453
页数：6
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