• 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

神经生长因子使新生大鼠纹状体中的胆碱乙酰转移酶活性增加。

Choline acetyltransferase activity in striatum of neonatal rats increased by nerve growth factor.

作者信息

Mobley W C, Rutkowski J L, Tennekoon G I, Buchanan K, Johnston M V

出版信息

Science. 1985 Jul 19;229(4710):284-7. doi: 10.1126/science.2861660.

DOI:10.1126/science.2861660
PMID:2861660
Abstract

Some neurodegenerative disorders may be caused by abnormal synthesis or utilization of trophic molecules required to support neuronal survival. A test of this hypothesis requires that trophic agents specific for the affected neurons be identified. Cholinergic neurons in the corpus striatum of neonatal rats were found to respond to intracerebroventricular administration of nerve growth factor with prominent, dose-dependent, selective increases in choline acetyltransferase activity. Cholinergic neurons in the basal forebrain also respond to nerve growth factor in this way. These actions of nerve growth factor may indicate its involvement in the normal function of forebrain cholinergic neurons as well as in neurodegenerative disorders involving such cells.

摘要

一些神经退行性疾病可能是由支持神经元存活所需的营养分子的异常合成或利用引起的。对这一假设的检验需要确定对受影响神经元具有特异性的营养因子。发现新生大鼠纹状体中的胆碱能神经元对脑室内给予神经生长因子有反应,胆碱乙酰转移酶活性显著、剂量依赖性地选择性增加。基底前脑的胆碱能神经元也以这种方式对神经生长因子作出反应。神经生长因子的这些作用可能表明它参与了前脑胆碱能神经元的正常功能以及涉及此类细胞的神经退行性疾病。

相似文献

1
Choline acetyltransferase activity in striatum of neonatal rats increased by nerve growth factor.神经生长因子使新生大鼠纹状体中的胆碱乙酰转移酶活性增加。
Science. 1985 Jul 19;229(4710):284-7. doi: 10.1126/science.2861660.
2
Differential effects of insulin on choline acetyltransferase and glutamic acid decarboxylase activities in neuron-rich striatal cultures.胰岛素对富含神经元的纹状体培养物中胆碱乙酰转移酶和谷氨酸脱羧酶活性的不同影响。
J Neurochem. 1992 Aug;59(2):415-24. doi: 10.1111/j.1471-4159.1992.tb09387.x.
3
Intrastriatal infusion of nerve growth factor after quinolinic acid prevents reduction of cellular expression of choline acetyltransferase messenger RNA and trkA messenger RNA, but not glutamate decarboxylase messenger RNA.喹啉酸注射后纹状体内注入神经生长因子可防止胆碱乙酰转移酶信使核糖核酸和trkA信使核糖核酸的细胞表达减少,但不能防止谷氨酸脱羧酶信使核糖核酸减少。
Neuroscience. 1994 Jul;61(2):257-68. doi: 10.1016/0306-4522(94)90229-1.
4
K-252a promotes survival and choline acetyltransferase activity in striatal and basal forebrain neuronal cultures.K-252a可促进纹状体和基底前脑神经元培养物的存活及胆碱乙酰转移酶活性。
J Neurochem. 1995 Apr;64(4):1502-12. doi: 10.1046/j.1471-4159.1995.64041502.x.
5
Long-term sequelae of striatal kainate lesion.纹状体红藻氨酸损伤的长期后遗症。
Brain Res. 1978 Sep 8;152(3):626-32. doi: 10.1016/0006-8993(78)91121-6.
6
Comparison of nerve growth factor's effects on development of septum, striatum, and nucleus basalis cholinergic neurons in vitro.神经生长因子对体外培养的隔区、纹状体及基底核胆碱能神经元发育影响的比较。
J Neurosci Res. 1988 Oct-Dec;21(2-4):352-64. doi: 10.1002/jnr.490210227.
7
The response of GABAergic and cholinergic neurons to transient cerebral ischemia.γ-氨基丁酸能神经元和胆碱能神经元对短暂性脑缺血的反应。
Brain Res. 1982 Jul 15;243(2):271-8. doi: 10.1016/0006-8993(82)90250-5.
8
Nerve growth factor increases choline acetyltransferase activity in developing basal forebrain neurons.神经生长因子可增加发育中的基底前脑神经元中的胆碱乙酰转移酶活性。
Brain Res. 1986 Jul;387(1):53-62. doi: 10.1016/0169-328x(86)90020-3.
9
Pharmacological characterization of nerve growth factor and/or monosialoganglioside GM1 effects on cholinergic markers in the adult lesioned brain.神经生长因子和/或单唾液酸神经节苷脂GM1对成年脑损伤后胆碱能标志物影响的药理学特性
J Pharmacol Exp Ther. 1995 Feb;272(2):527-45.
10
NGF-mediated increase of choline acetyltransferase (ChAT) in the neonatal rat forebrain: evidence for a physiological role of NGF in the brain?神经生长因子介导新生大鼠前脑胆碱乙酰转移酶(ChAT)的增加:神经生长因子在大脑中具有生理作用的证据?
Brain Res. 1983 Jul;285(1):45-52. doi: 10.1016/0165-3806(83)90107-4.

引用本文的文献

1
The Nerve Growth Factor Metabolic Pathway Dysregulation as Cause of Alzheimer's Cholinergic Atrophy.神经生长因子代谢途径失调是阿尔茨海默病胆碱能萎缩的原因。
Cells. 2021 Dec 22;11(1):16. doi: 10.3390/cells11010016.
2
Endogenous and exogenous opioid effects on oligodendrocyte biology and developmental brain myelination.内源性和外源性阿片样物质对少突胶质细胞生物学和发育中大脑髓鞘形成的影响。
Neurotoxicol Teratol. 2021 Jul-Aug;86:107002. doi: 10.1016/j.ntt.2021.107002. Epub 2021 Jun 12.
3
Rodent Models of Amyloid-Beta Feature of Alzheimer's Disease: Development and Potential Treatment Implications.
阿尔茨海默病β淀粉样蛋白特征的啮齿动物模型:建立与潜在治疗意义
Aging Dis. 2020 Oct 1;11(5):1235-1259. doi: 10.14336/AD.2019.1026. eCollection 2020 Oct.
4
Exploring the Pathogenesis of Alzheimer Disease in Basal Forebrain Cholinergic Neurons: Converging Insights From Alternative Hypotheses.探索基底前脑胆碱能神经元中阿尔茨海默病的发病机制:来自不同假说的综合见解
Front Neurosci. 2019 May 7;13:446. doi: 10.3389/fnins.2019.00446. eCollection 2019.
5
Treadmill exercise after social isolation increases the levels of NGF, BDNF, and synapsin I to induce survival of neurons in the hippocampus, and improves depression-like behavior.社交隔离后进行跑步机运动可提高神经生长因子、脑源性神经营养因子和突触素I的水平,以诱导海马体中神经元的存活,并改善抑郁样行为。
J Exerc Nutrition Biochem. 2015 Mar;19(1):11-8. doi: 10.5717/jenb.2015.19.1.11. Epub 2015 Mar 31.
6
Swimming exercise stimulates neuro-genesis in the subventricular zone via increase in synapsin I and nerve growth factor levels.游泳运动通过增加突触结合蛋白 I 和神经生长因子水平来刺激侧脑室下区的神经发生。
Biol Sport. 2014 Dec;31(4):309-14. doi: 10.5604/20831862.1132130. Epub 2014 Oct 16.
7
Alleviating effects of Bushen-Yizhi formula on ibotenic acid-induced cholinergic impairments in rat.补肾益智方对鹅膏蕈氨酸诱导的大鼠胆碱能损伤的缓解作用。
Rejuvenation Res. 2015 Apr;18(2):111-27. doi: 10.1089/rej.2014.1603.
8
Acute and chronic administration of the branched-chain amino acids decreases nerve growth factor in rat hippocampus.急性和慢性给予支链氨基酸可降低大鼠海马神经生长因子。
Mol Neurobiol. 2013 Dec;48(3):581-9. doi: 10.1007/s12035-013-8447-1. Epub 2013 Apr 5.
9
NGF, brain and behavioral plasticity.神经生长因子、大脑和行为可塑性。
Neural Plast. 2012;2012:784040. doi: 10.1155/2012/784040. Epub 2012 Feb 16.
10
TrkA gene ablation in basal forebrain results in dysfunction of the cholinergic circuitry.基底前脑中 TrkA 基因的缺失导致胆碱能回路功能障碍。
J Neurosci. 2012 Mar 21;32(12):4065-79. doi: 10.1523/JNEUROSCI.6314-11.2012.