南方医科大学学报

南方医科大学学报 ›› 2004, Vol. 24 ›› Issue (04): 461-463,466.

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N-甲基-D-天门冬氨酸受体介导缺氧SD大鼠PO/AH区神经元Ca2+浓度的变化

赵庆平1, 邹飞2, 陈光忠1, 李铁林1   

  1. 1. 第一军医大学珠江医院神经外科, 广东, 广州, 510282;
    2. 第一军医大学热带军队卫生学系高温医学研究室, 广东, 广州, 510515
  • 出版日期:2004-04-20 发布日期:2004-04-20
  • 基金资助:
    收稿日期:2003-9-18。
    作者简介:赵庆平(1964-),男,主治医师,在读博士,电话:020-61643263

Changes in Ca2+ concentration mediated by N-methyl-D-aspartate receptor in PO/AH neurons of anoxic SD rats

ZHAO Qing-ping1, ZOU Fei2, CHEN Guang-zhong1, LI Tie-lin1   

  1. 1. 第一军医大学珠江医院神经外科, 广东, 广州, 510282;
    2. 第一军医大学热带军队卫生学系高温医学研究室, 广东, 广州, 510515
  • Online:2004-04-20 Published:2004-04-20

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摘要： 目的 研究N-甲基-D-天门冬氨酸(NMDA)受体特性,探讨NMDA对缺氧大鼠PO/AH区神经元Ca2+浓度的影响。方法 给大鼠应用NMDA受体激动剂NMDA和拮抗剂丙戊酸,观察其在正常和缺氧条件下对PO/AH区神经细胞内Ca2+浓度的影响。结果 在正常条件下,细胞内Ca2+荧光比值为0.95,第40秒加入NMDA后[Ca2+]i的荧光强度迅速增高,25s后达到峰值2.054,并稳定在此水平,其升幅为(109±52)%,加入激动剂后30 s内达到峰值3.783,并持续稳定在此水平,加入NMDA后[Ca2+]i升高了(286±91)%;缺氧条件下神经元[Ca2+]i在加入丙戌酸后由平台向下的降幅为(103±45)%。结论 [Ca2+]i的升高主要是由于NMDA受体通道开放,细胞外游离Ca2+易化扩散入胞内所致,丙戊酸可有效地降低NMDA受体活性,从而使细胞内游离Ca2+浓度明显下降,具有保护神经元免受缺氧损伤的作用。

Abstract: Objective To study the changes of Ca2+ concentration mediated by N-methyl-D-aspartate (NMDA) receptor in the neurons in the preoptic area/anterior hypothalamus (PO/AH) of anoxic SD rats by investigating the properties of NMDA receptor. Methods The effects of NMDA receptor agonist NMDA and antagonist vaproic acid (VPA) on the[Ca2+]i in PO/AH neurons were observed in SD rats with anoxia. Results Under normal condition, the fluorescencet ratio was 0.95, which increased obviously in response to treatment with NMDA at 40 s and reached the peak value, 2.054, after 25 s with an increment of (109±52)%. After the addition of the agonist, the peak value reached 3.783 in 30 s and maintained the high level. The concentration of Ca2+ increased by (286±91)% after the treatment with NMDA. While in the anoxia group, the concentration of Ca2+ decreased by (103±45)% after the addition of VPA. Conclusions The increase in the concentration of Ca2+ results predominantly from the opening of NMDA receptor channel which allows Ca2+ influx. VPA may decrease the activity of NMDA receptor to reduce the Ca2+ concentration for the protection of the neurons against anoxia.

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