脂多糖对运动神经末梢递质自发释放的体内效应。
The in vivo effect of lipopolysaccharide on the spontaneous release of transmitter from motor nerve terminals.
作者信息
Liu S H, Sheu T J, Lin R H, Lin-Shiau S Y
机构信息
Institute of Toxicology, College of Medicine, National Taiwan University, Taipei.
出版信息
Br J Pharmacol. 1995 Sep;116(2):1757-60. doi: 10.1111/j.1476-5381.1995.tb16659.x.
Abstract
- The in vivo effect of E. coli lipopolysaccharide (LPS) on the spontaneous release of transmitter was studied in the isolated phrenic nerve-diaphragm preparation of the mouse. 2. The resting membrane potential was decreased and frequency of miniature endplate potentials (m.e.p.ps) was increased by treatment with LPS. 3. Pretreatment of diaphragms with ouabain markedly increased the frequency of m.e.p.ps in control group but not in the LPS group. 4. When mice were treated with polymyxin B (a LPS neutralizer), pentoxifylline (an inhibitor of tumor necrosis factor-alpha formation) and NG-nitro-L-arginine (an inhibitor of nitric oxide (NO) synthase) the effects of LPS were reversed. 5. These results suggest that LPS increases the spontaneous transmitter release through, at least in part, the pathways of tumour necrosis factor-alpha and NO followed by an inhibition of the Na(+)-pump activity in the endplate area.
摘要
- 在小鼠膈神经-膈肌离体标本中研究了大肠杆菌脂多糖（LPS）对递质自发释放的体内作用。2. LPS处理可降低静息膜电位并增加微小终板电位（m.e.p.ps）的频率。3. 用哇巴因预处理膈肌，对照组m.e.p.ps频率显著增加，而LPS组无此现象。4. 当用多粘菌素B（一种LPS中和剂）、己酮可可碱（一种肿瘤坏死因子-α形成抑制剂）和NG-硝基-L-精氨酸（一种一氧化氮（NO）合酶抑制剂）处理小鼠时，LPS的作用被逆转。5. 这些结果表明，LPS至少部分通过肿瘤坏死因子-α和NO途径增加递质的自发释放，随后抑制终板区的Na(+)-泵活性。
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本文引用的文献
1
An analysis of the end-plate potential recorded with an intracellular electrode.用细胞内电极记录的终板电位分析。
J Physiol. 1951 Nov 28;115(3):320-70. doi: 10.1113/jphysiol.1951.sp004675.
2
Inhibition of endogenous TNF formation by pentoxifylline.己酮可可碱对内源性肿瘤坏死因子形成的抑制作用。
Immunobiology. 1993 Apr;187(3-5):447-63. doi: 10.1016/S0171-2985(11)80356-6.
3
Interferon-alpha, beta and tumor necrosis factor-alpha enhance the frequency of miniature end-plate potentials at rat neuromuscular junction.α干扰素、β干扰素和肿瘤坏死因子α可提高大鼠神经肌肉接头处微小终板电位的频率。
Neurosci Lett. 1994 Jan 17;166(1):97-100. doi: 10.1016/0304-3940(94)90849-4.
4
Synthesis of nitric oxide in CNS glial cells.中枢神经系统神经胶质细胞中一氧化氮的合成。
Trends Neurosci. 1993 Aug;16(8):323-8. doi: 10.1016/0166-2236(93)90109-y.
5
Tumor necrosis factor-alpha (TNF-alpha), interferon-gamma, and interleukin-6 but not TNF-beta induce differentiation of neuroblastoma cells: the role of nitric oxide.肿瘤坏死因子-α（TNF-α）、干扰素-γ和白细胞介素-6可诱导神经母细胞瘤细胞分化，但肿瘤坏死因子-β不能：一氧化氮的作用。
J Neurochem. 1994 Apr;62(4):1330-6. doi: 10.1046/j.1471-4159.1994.62041330.x.
6
Prevention of the generalized Shwartzman reaction and endotoxin lethality by polymyxin B localized in tissues.多粘菌素B定位于组织中对全身性施瓦茨曼反应和内毒素致死性的预防作用
Infect Immun. 1974 Aug;10(2):287-92. doi: 10.1128/iai.10.2.287-292.1974.
7
Stimulation, by inhibition of (Na + -K + -Mg 2+ )-activated ATP-ase, of acetylcholine release in cortical slices from rat brain.通过抑制（钠+-钾+-镁2+）激活的ATP酶刺激大鼠脑皮质切片中乙酰胆碱的释放。
J Physiol. 1972 Oct;226(1):95-117. doi: 10.1113/jphysiol.1972.sp009975.
8
Secretory products of macrophages.巨噬细胞的分泌产物。
J Clin Invest. 1987 Feb;79(2):319-26. doi: 10.1172/JCI112815.
9
Tumor necrosis, cachexia, shock, and inflammation: a common mediator.肿瘤坏死、恶病质、休克与炎症：一种共同介质。
Annu Rev Biochem. 1988;57:505-18. doi: 10.1146/annurev.bi.57.070188.002445.
10
Nitric oxide. A macrophage product responsible for cytostasis and respiratory inhibition in tumor target cells.一氧化氮。一种巨噬细胞产物，负责肿瘤靶细胞中的细胞停滞和呼吸抑制。
J Exp Med. 1989 May 1;169(5):1543-55. doi: 10.1084/jem.169.5.1543.
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