• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

缺氧神经末梢中糖酵解维持功能的失败。

Failure to maintain glycolysis in anoxic nerve terminals.

作者信息

Kauppinen R A, Nicholls D G

出版信息

J Neurochem. 1986 Dec;47(6):1864-9. doi: 10.1111/j.1471-4159.1986.tb13100.x.

DOI:10.1111/j.1471-4159.1986.tb13100.x
PMID:3095495
Abstract

Synaptosomal glycolysis is stimulated eight- to 10-fold when the respiratory chain is inhibited by cyanide or by anoxia. However, the stimulation is transient and after 15 min declines toward the preanoxic rate. The decline is not seen when Ca2+ is absent or when the respiratory chain is inhibited by rotenone. The decline in glycolysis is reversible, is not due to substrate exhaustion, and is the cause, rather than the effect, of lowered synaptosomal ATP/ADP ratios. The failure to maintain glycolysis when the terminal oxidase of the respiratory chain is inhibited may have relevance to the sensitivity of the brain to anoxic damage.

摘要

当呼吸链被氰化物或缺氧抑制时,突触体糖酵解被刺激8到10倍。然而,这种刺激是短暂的,15分钟后朝着缺氧前的速率下降。当不存在Ca2+或呼吸链被鱼藤酮抑制时,这种下降就不会出现。糖酵解的下降是可逆的,不是由于底物耗尽,并且是突触体ATP/ADP比率降低的原因而非结果。当呼吸链的末端氧化酶被抑制时无法维持糖酵解,这可能与大脑对缺氧损伤的敏感性有关。

相似文献

1
Failure to maintain glycolysis in anoxic nerve terminals.缺氧神经末梢中糖酵解维持功能的失败。
J Neurochem. 1986 Dec;47(6):1864-9. doi: 10.1111/j.1471-4159.1986.tb13100.x.
2
Anaerobic glycolysis and postanoxic recovery of respiration of rat cortical synaptosomes are reduced by synaptosomal sodium load.突触体钠负荷会降低大鼠皮质突触体的无氧糖酵解和缺氧后呼吸恢复。
Brain Res. 1993 May 21;611(2):286-94. doi: 10.1016/0006-8993(93)90515-o.
3
Plasma membrane depolarization and disturbed Na+ homeostasis induced by the protonophore carbonyl cyanide-p-trifluoromethoxyphenyl-hydrazon in isolated nerve terminals.质子载体羰基氰化物 - 对 - 三氟甲氧基苯腙在离体神经末梢中诱导的质膜去极化和钠稳态紊乱。
Mol Pharmacol. 1998 Apr;53(4):734-41. doi: 10.1124/mol.53.4.734.
4
Ca2+-dependent and Ca2+-independent glutamate release, energy status and cytosolic free Ca2+ concentration in isolated nerve terminals following metabolic inhibition: possible relevance to hypoglycaemia and anoxia.代谢抑制后分离神经末梢中钙依赖型和非钙依赖型谷氨酸释放、能量状态及胞质游离钙浓度:与低血糖和缺氧的可能关联
Neuroscience. 1988 Oct;27(1):175-82. doi: 10.1016/0306-4522(88)90228-x.
5
Differential effects of respiratory inhibitors on glycolysis in proximal tubules.呼吸抑制剂对近端小管糖酵解的不同作用
Am J Physiol. 1990 Jun;258(6 Pt 2):F1608-15. doi: 10.1152/ajprenal.1990.258.6.F1608.
6
Effects of metabolic blockers on Ca(2+)-dependent currents in cultured sensory neurones from neonatal rats.代谢阻滞剂对新生大鼠培养感觉神经元中钙依赖性电流的影响。
Br J Pharmacol. 1994 Jan;111(1):57-64. doi: 10.1111/j.1476-5381.1994.tb14023.x.
7
Neuroprotection by lowering cholesterol: a decrease in membrane cholesterol content reduces transporter-mediated glutamate release from brain nerve terminals.通过降低胆固醇实现神经保护:膜胆固醇含量的降低减少了转运体介导的谷氨酸从脑神经末梢的释放。
Biochim Biophys Acta. 2012 Oct;1822(10):1553-61. doi: 10.1016/j.bbadis.2012.06.005. Epub 2012 Jun 17.
8
Control of intracellular calcium in presynaptic nerve terminals.突触前神经末梢内钙离子的调控
Fed Proc. 1980 Aug;39(10):2790-5.
9
Calcium buffering in presynaptic nerve terminals. Free calcium levels measured with arsenazo III.突触前神经末梢中的钙缓冲。用偶氮胂III测量游离钙水平。
Biochim Biophys Acta. 1980 Aug 14;600(3):912-21. doi: 10.1016/0005-2736(80)90493-9.
10
ATP depletion increases Ca2+ uptake by synaptosomes.三磷酸腺苷(ATP)耗竭会增加突触体对钙离子(Ca2+)的摄取。
FEBS Lett. 1981 Nov 30;135(1):212-4. doi: 10.1016/0014-5793(81)80979-9.

引用本文的文献

1
Complex I Controls Mitochondrial and Plasma Membrane Potentials in Nerve Terminals.复合物 I 控制神经末梢中的线粒体和质膜电势。
Neurochem Res. 2021 Jan;46(1):100-107. doi: 10.1007/s11064-020-02990-8. Epub 2020 Mar 4.
2
Bioenergetics and redox adaptations of astrocytes to neuronal activity.星形胶质细胞对神经元活动的生物能量学和氧化还原适应性
J Neurochem. 2016 Oct;139 Suppl 2(Suppl Suppl 2):115-125. doi: 10.1111/jnc.13486. Epub 2016 Mar 10.
3
Brain lactate metabolism: the discoveries and the controversies.脑乳酸代谢:发现与争议。
J Cereb Blood Flow Metab. 2012 Jul;32(7):1107-38. doi: 10.1038/jcbfm.2011.175. Epub 2011 Dec 21.
4
Multiple Ca2+-dependent mechanisms regulate L-type Ca2+ current in retinal amacrine cells.多种依赖 Ca2+ 的机制调节视网膜无长突细胞中的 L 型 Ca2+ 电流。
J Neurophysiol. 2010 Oct;104(4):1849-66. doi: 10.1152/jn.00031.2010. Epub 2010 Aug 4.
5
Mitochondrial complex II prevents hypoxic but not calcium- and proapoptotic Bcl-2 protein-induced mitochondrial membrane potential loss.线粒体复合物 II 可防止缺氧诱导的,但不能防止钙和促凋亡 Bcl-2 蛋白诱导的线粒体膜电位丧失。
J Biol Chem. 2010 Aug 20;285(34):26494-505. doi: 10.1074/jbc.M110.143164. Epub 2010 Jun 21.
6
Bioenergetic analysis of isolated cerebrocortical nerve terminals on a microgram scale: spare respiratory capacity and stochastic mitochondrial failure.微克级分离脑皮质神经末梢的生物能量分析:备用呼吸能力和随机线粒体功能衰竭
J Neurochem. 2009 May;109(4):1179-91. doi: 10.1111/j.1471-4159.2009.06055.x. Epub 2009 Mar 23.
7
Alois Alzheimer revisited: differences in origin of the disease carrying his name.重温阿洛伊斯·阿尔茨海默:以他名字命名的疾病的起源差异。
J Neural Transm (Vienna). 2006 Nov;113(11):1645-58. doi: 10.1007/s00702-006-0592-5. Epub 2006 Oct 23.
8
Complex interplay between glutamate receptors and intracellular Ca2+ stores during ischaemia in rat spinal cord white matter.大鼠脊髓白质缺血期间谷氨酸受体与细胞内钙库之间的复杂相互作用。
J Physiol. 2006 Nov 15;577(Pt 1):191-204. doi: 10.1113/jphysiol.2006.116798. Epub 2006 Aug 31.
9
The production of reactive oxygen species in intact isolated nerve terminals is independent of the mitochondrial membrane potential.完整分离的神经末梢中活性氧的产生与线粒体膜电位无关。
Neurochem Res. 2003 Oct;28(10):1575-81. doi: 10.1023/a:1025634728227.
10
Aberrant chloride transport contributes to anoxic/ischemic white matter injury.异常的氯离子转运导致缺氧/缺血性白质损伤。
J Neurosci. 2003 May 1;23(9):3826-36. doi: 10.1523/JNEUROSCI.23-09-03826.2003.