期刊文献+

Effect of Morphine and Naloxone on Release of the Excitatory Amino Acids of Spinal Astrocytes Induced by TNF-α 被引量:2

Effect of Morphine and Naloxone on Release of the Excitatory Amino Acids of Spinal Astrocytes Induced by TNF-α
下载PDF
导出
摘要 The effect of morphine and naloxone on release of the excitatory amino acids (EAAs) of spinal astrocytes induced by TNF-α was studied. Astrocytes were purified from 2- to 3-day old SD rats and divided into 8 groups: group 1 (without any stimulatants); group 2 (10 ng/ml TNF-α); group3 (10 ng/ml TNF-α+0.5 μmol/L morphine); group 4 (10 ng/ml TNF-α+1.0 μmol/L morphine); group 5 (10 ng/ml TNF-α+2.0 μmol/L morphine); group 6 (10 ng/ml TNF-α+0.5 μmol/L naloxone); group 7 (10 ng/ml TNF-α+1.0 μmol/L naloxone); group 8 (10 ng/ml TNF-α+2.0 μmol/L naloxone). In group 2, 3, 4 and 5, 0, 0.5, 1.0 or 2.0 μmol/L morphine was added to the cells cultured with serum-free Neurobasal/B27 medium containing 10 ng/ml TNF-α respectively, while in group 6, 7 and 8, 0.5, 1.0 or 2.0 μmol/L naloxone was added respectively to the cells cultured with serum-free Neurobasal/B27 medium containing 10 ng/ml TNF-α. After 30 min incubation, high-pressure liquid chromatography (HPLC) was used to measure the levels of EAAs in all cultured cells. The results showed the level of EAAs in group 2 was significant higher than in group 1 (P<0.01). As compared with group 2, the levels of EAAs in group 3, 4 and 5 were decreased with the difference being significant between group 5 and group 2 (P<0.01) or between group 4 and group 2 (P<0.05). The levels of EAAs in group 6, 7 and group 8 was significantly lower than in group 2 (P<0.05 or P<0.01). It was concluded that TNF-α could promote the release of glutamate and aspartate from astrocytes, and morphine and naloxone might reduce the release of EAAs in cultured spinal astrocytes induced by TNF-α. The effect of morphine and naloxone on release of the excitatory amino acids (EAAs) of spinal astrocytes induced by TNF-α was studied. Astrocytes were purified from 2- to 3-day old SD rats and divided into 8 groups: group 1 (without any stimulatants); group 2 (10 ng/ml TNF-α); group3 (10 ng/ml TNF-α+0.5 μmol/L morphine); group 4 (10 ng/ml TNF-α+1.0 μmol/L morphine); group 5 (10 ng/ml TNF-α+2.0 μmol/L morphine); group 6 (10 ng/ml TNF-α+0.5 μmol/L naloxone); group 7 (10 ng/ml TNF-α+1.0 μmol/L naloxone); group 8 (10 ng/ml TNF-α+2.0 μmol/L naloxone). In group 2, 3, 4 and 5, 0, 0.5, 1.0 or 2.0 μmol/L morphine was added to the cells cultured with serum-free Neurobasal/B27 medium containing 10 ng/ml TNF-α respectively, while in group 6, 7 and 8, 0.5, 1.0 or 2.0 μmol/L naloxone was added respectively to the cells cultured with serum-free Neurobasal/B27 medium containing 10 ng/ml TNF-α. After 30 min incubation, high-pressure liquid chromatography (HPLC) was used to measure the levels of EAAs in all cultured cells. The results showed the level of EAAs in group 2 was significant higher than in group 1 (P<0.01). As compared with group 2, the levels of EAAs in group 3, 4 and 5 were decreased with the difference being significant between group 5 and group 2 (P<0.01) or between group 4 and group 2 (P<0.05). The levels of EAAs in group 6, 7 and group 8 was significantly lower than in group 2 (P<0.05 or P<0.01). It was concluded that TNF-α could promote the release of glutamate and aspartate from astrocytes, and morphine and naloxone might reduce the release of EAAs in cultured spinal astrocytes induced by TNF-α.
出处 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2005年第1期91-93,共3页 华中科技大学学报(医学英德文版)
关键词 tumor necrosis factor-α ASTROCYTE GLUTAMATE ASPARTATE NALOXONE MORPHINE tumor necrosis factor-α astrocyte glutamate aspartate naloxone morphine
  • 相关文献

参考文献7

  • 1刘庆莹,朱长庚,赵珠峰.TNFα刺激的星形胶质细胞条件培养液对海马神经元的兴奋作用[J].解剖学杂志,2002,25(3):205-209. 被引量:5
  • 2Watkins,L R,Milligan,E D,Maier,S F.Glial activation: a driving force for pathological pain[].Trends in Neurosciences.2001
  • 3McCarthy,K D,Devellis,J.Preparation of separate astroglial and oligodendroglial cultures from rat cerebral tissue[].The Journal of Cell Biology.1980
  • 4Watkins,L R,Milligan,E D,Maier,S F.Spinal cord glial: new players in pain[].Pain.2001
  • 5Bianchi L,Colivicchi M A,Bolam J P et al.The release of amino acids from rat neostriatum and substantia nigra in vivo: a dual microdialysis probe analysis[].Neuroscience.1998
  • 6Hopkins S J,Rothwell N J.Cytokines and the nervous system.I: Expression and recognition[].Trends in Neurosciences.1995
  • 7Diehl,J A,Tong,W,Sun,G.Tumor necrosis factor-alpha-dependent activation of a RelA homodimer in astrocytes. Increased phosphorylation of RelA and MAD-3 precede activation of RelA[].Journal of Biological Chemistry.1995

二级参考文献12

  • 1[1]Steinhauser C,Gallo V.News on glutamate receptors in glial cells.Trends Neurosci,1996,19 (8):339345.
  • 2[2]Parpura V,Basarsky TA,Liu F,et al.Glutamate mediated astrocyte-neuron signaling.Nature,1994,369(6483):744-747.
  • 3[3]Hopkins SJ,Rothwell NJ.Cytokines in the nervous system I:expression and recognition.Trends Neurosci,1995,18(2):83-88.
  • 4[4]Koller H,Thiem K,Siebler M.Tumor necrosis fac tor-α increases intracellular Ca2 + and induces a depolarization in cultured astroglial cells.Brain,1996,119 (6):2021-2027.
  • 5[5]McCarthy KD,DeVellis J.Preparation of separate astroglial and oligodendroglial cultures from rat cerebral tissue J Cell Biol,1980,85(3):890-902.
  • 6[6]Longuemare MC,Rose CR,Farrell K,et al.K + -induced reversal of astrocyte glutamate uptake is limited by compensatory changes in intracellular Na+.Neuroscience,1999,93 (1):285-292.
  • 7[7]Choi DW,Koh JY.Quantitative detenmination of glutamate mediated cortical neuronal injury in cell culture by Lactate Dehydrogenase efflux assay.J Nevi Method,1987,20(1):83-90.
  • 8[8]KollerH,AllertN,OelD,etal.TNFalphainducesa protein kinase C-dependent reduction in astroglial K+ conductance.Neuroreport,1998,9(7):1375-1378.
  • 9[9]Szymocha R,Akaoka H,Dutuit M,et al.Human Tcell lymphotropic virus type l-infected T lymphocytes impair catabolim and uptake of glutamate by astrocytes via Tax-1 and tumor necrosis factor alpha.J Virol,2000,74(14):6433-6441.
  • 10[10]O' Neill LA,Kaltschmidt C.NF-κ B:a crucial transcription factor for glial and neuronal cell function.Trends Neurosci,1997,20 (6):252-258.

共引文献4

同被引文献3

引证文献2

二级引证文献5

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部