中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2015, Vol. 10 ›› Issue (7): 1095-1100.doi: 10.4103/1673-5374.160101

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

孕期乙醇暴露对新生大鼠延髓前包钦格复合体神经元的神经毒性

  

  • 收稿日期:2015-05-07 出版日期:2015-07-24 发布日期:2015-07-24
  • 基金资助:

    河南省自然基金 (102102310156)

Neurotoxicity of prenatal alcohol exposure on medullary pre-Bötzinger complex neurons in neonatal rats

Ming-li Ji 1, Yun-hong Wu 2, Zhi-bin Qian 2   

  1. 1 Department of Physiology, Xinxiang Medical University, Xinxiang, Henan Province, China
    2 Department of Functional Laboratory, Xinxiang Medical University, Xinxiang, Henan Province, China
  • Received:2015-05-07 Online:2015-07-24 Published:2015-07-24
  • Contact: Zhi-bin Qian, Ph.D., qianzhibin@126.com.
  • Supported by:

    This work was supported by the Natural Science Foundation of Henan Province in China, No. 102102310156; the Foundation of Xinxiang Technology Bureau in China, No. ZG14004.

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摘要：

孕期乙醇暴露抑制胎儿延髓呼吸功能，但是否抑制基本节律性呼吸放电，5-羟色胺2A受体是否参与该抑制作用目前尚不清楚。为明确此问题，实验在大鼠整个孕期分别给予0%, 1%, 2%, 4%, 8%, 10% (v/v) 乙醇水溶液作为各组大鼠惟一饮用水源。使用出生2 d的新生大鼠用于制备延髓脑片，记录基本节律性呼吸放电。使用Western blot 和qRT-PCR方法检测孕期乙醇暴露对前包钦格复合体神经元5-羟色胺2A受体蛋白及其mRNA表达水平的影响。4%，8%和10%乙醇孕期暴露组新生大鼠基本节律性呼吸放电减弱，8%组基本节律性呼吸放电降低最显著，10%组基本节律性呼吸放电虽然比8%组更弱，但基本节律性呼吸放电变得不规则，所以8%的乙醇水溶液是复制孕期乙醇暴露对新生大鼠基本节律性呼吸放电作用动物模型的最适浓度。实验结果提示，孕期乙醇暴露通过下调延髓前包钦格复合体神经元5-羟色胺2A受体及其mRNA表达，进而起到抑制新生大鼠基本节律性呼吸放电的作用。

关键词: 神经再生, 脑损伤, 产前乙醇暴露, 呼吸抑制, 新生大鼠, 髓质层, 呼吸性放电活动, Bötzinger复合体, 延髓呼吸中枢, 呼吸神经元, 5-HT2A受体

Abstract:

Prenatal alcohol exposure disrupts the development of normal fetal respiratory function, but whether it perturbs respiratory rhythmical discharge activity is unclear. Furthermore, it is unknown whether the 5-hydroxytryptamine 2A receptor (5-HT2AR) is involved in the effects of prenatal alcohol exposure. In the present study, pregnant female rats received drinking water containing alcohol at concentrations of 0%, 1%, 2%, 4%, 8% or 10% (v/v) throughout the gestation period. Slices of the medulla from 2-day-old neonatal rats were obtained to record respiratory rhythmical discharge activity. 5-HT2AR protein and mRNA levels in the pre-Bötzinger complex of the respiratory center were measured by western blot analysis and quantitative RT-PCR, respectively. Compared with the 0% alcohol group, respiratory rhythmical discharge activity in medullary slices in the 4%, 8% and 10% alcohol groups was decreased, and the reduction was greatest in the 8% alcohol group. Respiratory rhythmical discharge activity in the 10% alcohol group was irregular. Thus, 8% was the most effective alcohol concentration at attenuating respiratory rhythmical discharge activity. These findings suggest that prenatal alcohol exposure attenuates respiratory rhythmical discharge activity in neonatal rats by downregulating 5-HT2AR protein and mRNA levels.

Key words: nerve regeneration, brain injury, prenatal alcohol exposure, pre-Bötzinger complex, respiratory depression, neonatal rats, medullary slice, medullary respiratory center, respiratory rhythmical discharge activity, respiratory neuron, 5-hydroxytryptamine 2A receptor, neural regeneration