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暴露于梭曼的神经节神经元中阿托品治疗前后的比较。

Comparison of atropine pre- and post-treatment in ganglion neurons exposed to soman.

作者信息

Heppner T J, Fiekers J F

机构信息

Department of Anatomy and Neurobiology, University of Vermont, College of Medicine, Burlington 05405.

出版信息

Brain Res Bull. 1992 Jun;28(6):849-52. doi: 10.1016/0361-9230(92)90204-b.

DOI:10.1016/0361-9230(92)90204-b
PMID:1638413
Abstract

The prevention and reversal of the effects of soman (pinacoloxymethylphosporyl fluoride) have been examined on the electrical properties of sympathetic ganglion neurons in vitro from the adult bullfrog Rana catesbeiana. Atropine (10 microM) pre-treatment (before soman) blocked the soman-induced decrease in the membrane potential, membrane resistance, and afterhyperpolarization (AHP) duration. Atropine post-treatment (after soman exposure) restored the soman-induced decrease in the membrane potential but was ineffective in reversing either the membrane resistance or the duration of the AHP. These results demonstrate: 1) that the effects of soman on the electrical properties of these neurons are mediated by the activation of muscarinic receptors, 2) that following receptor activation different cellular mechanisms may be involved in the regulation of the electrical properties of the neuron, and 3) pre-treatment rather than post-treatment with atropine is more effective in blocking these direct effects of soman. These results are discussed in reference to the increased effectiveness of atropine pretreatment in the protocols for soman-induced neurotoxicity.

摘要

已经对来自成年牛蛙(牛蛙)的体外交感神经节神经元的电特性进行了梭曼(频哪基甲基磷酰氟)作用的预防和逆转研究。阿托品(10微摩尔)预处理(在梭曼之前)可阻断梭曼诱导的膜电位、膜电阻和超极化后电位(AHP)持续时间的降低。阿托品后处理(在接触梭曼之后)恢复了梭曼诱导的膜电位降低,但在逆转膜电阻或AHP持续时间方面无效。这些结果表明:1)梭曼对这些神经元电特性的作用是由毒蕈碱受体的激活介导的;2)受体激活后,不同的细胞机制可能参与神经元电特性的调节;3)阿托品预处理而非后处理在阻断梭曼的这些直接作用方面更有效。参考梭曼诱导神经毒性方案中阿托品预处理有效性的提高对这些结果进行了讨论。

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