• 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

DREAM 调节 BDNF 依赖性脊髓致敏。

DREAM regulates BDNF-dependent spinal sensitization.

机构信息

Department of Physiology, Faculty of Medicine, University of Alcala, Madrid, Spain.

出版信息

Mol Pain. 2010 Dec 18;6:95. doi: 10.1186/1744-8069-6-95.

DOI:10.1186/1744-8069-6-95
PMID:21167062
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3027194/
Abstract

BACKGROUND

The transcriptional repressor DREAM (downstream regulatory element antagonist modulator) controls the expression of prodynorphin and has been involved in the modulation of endogenous responses to pain. To investigate the role of DREAM in central mechanisms of pain sensitization, we used a line of transgenic mice (L1) overexpressing a Ca(2+)- and cAMP-insensitive DREAM mutant in spinal cord and dorsal root ganglia.

RESULTS

L1 DREAM transgenic mice showed reduced expression in the spinal cord of several genes related to pain, including prodynorphin and BDNF (brain-derived neurotrophic factor) and a state of basal hyperalgesia without change in A-type currents. Peripheral inflammation produced enhancement of spinal reflexes and increased expression of BDNF in wild type but not in DREAM transgenic mice. The enhancement of the spinal reflexes was reproduced in vitro by persistent electrical stimulation of C-fibers in wild type but not in transgenic mice. Exposure to exogenous BDNF produced a long-term enhancement of dorsal root-ventral root responses in transgenic mice.

CONCLUSIONS

Our results indicate that endogenous BDNF is involved in spinal sensitization following inflammation and that blockade of BDNF induction in DREAM transgenic mice underlies the failure to develop spinal sensitization.

摘要

背景

转录抑制因子 DREAM（下游调节元件拮抗剂调节剂）控制着前脑啡肽原的表达，并参与了内源性疼痛反应的调节。为了研究 DREAM 在疼痛敏化的中枢机制中的作用，我们使用了一种在脊髓和背根神经节中过度表达钙（Ca 2+）和环腺苷酸（cAMP）不敏感的 DREAM 突变体的转基因小鼠（L1）系。

结果

L1 DREAM 转基因小鼠的脊髓中几种与疼痛相关的基因表达减少，包括前脑啡肽原和脑源性神经营养因子（BDNF），并且存在基础痛觉过敏而 A 型电流没有变化。外周炎症导致野生型小鼠脊髓反射增强和 BDNF 表达增加，但 DREAM 转基因小鼠则没有。在野生型小鼠中，持续电刺激 C 纤维可重现脊髓反射的增强，但在转基因小鼠中则不能。外源性 BDNF 的暴露导致转基因小鼠背根-腹根反应的长期增强。

结论

我们的结果表明，内源性 BDNF 参与了炎症后的脊髓敏化，而 DREAM 转基因小鼠中 BDNF 诱导的阻断是其脊髓敏化失败的基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82db/3027194/49823d28f721/1744-8069-6-95-8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82db/3027194/6a3d0e4a00e6/1744-8069-6-95-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82db/3027194/29cd63a19fda/1744-8069-6-95-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82db/3027194/4fd21dc55d5c/1744-8069-6-95-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82db/3027194/43f23b90bde4/1744-8069-6-95-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82db/3027194/857c068e1500/1744-8069-6-95-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82db/3027194/1f7aac8a388e/1744-8069-6-95-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82db/3027194/d8fe5c839acb/1744-8069-6-95-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82db/3027194/49823d28f721/1744-8069-6-95-8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82db/3027194/6a3d0e4a00e6/1744-8069-6-95-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82db/3027194/29cd63a19fda/1744-8069-6-95-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82db/3027194/4fd21dc55d5c/1744-8069-6-95-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82db/3027194/43f23b90bde4/1744-8069-6-95-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82db/3027194/857c068e1500/1744-8069-6-95-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82db/3027194/1f7aac8a388e/1744-8069-6-95-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82db/3027194/d8fe5c839acb/1744-8069-6-95-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/82db/3027194/49823d28f721/1744-8069-6-95-8.jpg

相似文献

1
DREAM regulates BDNF-dependent spinal sensitization.DREAM 调节 BDNF 依赖性脊髓致敏。
Mol Pain. 2010 Dec 18;6:95. doi: 10.1186/1744-8069-6-95.
2
Transcriptional repressor DREAM regulates trigeminal noxious perception.转录抑制因子DREAM调节三叉神经痛觉。
J Neurochem. 2017 May;141(4):544-552. doi: 10.1111/jnc.13584. Epub 2017 Feb 21.
3
Ifenprodil Reduced Expression of Activated Microglia, BDNF and DREAM Proteins in the Spinal Cord Following Formalin Injection During the Early Stage of Painful Diabetic Neuropathy in Rats.异佛尔酮衍生物减少糖尿病神经病理性疼痛大鼠早期福尔马林注射后脊髓内小胶质细胞激活、BDNF 和 DREAM 蛋白的表达。
J Mol Neurosci. 2021 Feb;71(2):379-393. doi: 10.1007/s12031-020-01661-1. Epub 2020 Jul 15.
4
Ca2+-dependent regulation of calcitonin gene expression by the transcriptional repressor DREAM.转录抑制因子DREAM对降钙素基因表达的钙离子依赖性调控
Endocrinology. 2006 Oct;147(10):4608-17. doi: 10.1210/en.2006-0254. Epub 2006 Jul 13.
5
Expressions of spinal microglia activation, BDNF, and DREAM proteins correlated with formalin-induced nociceptive responses in painful and painless diabetic neuropathy rats.脊髓小胶质细胞激活、BDNF 和 DREAM 蛋白的表达与痛性和无痛性糖尿病神经病变大鼠福尔马林诱导的痛觉反应相关。
Neuropeptides. 2020 Feb;79:102003. doi: 10.1016/j.npep.2019.102003. Epub 2019 Dec 24.
6
Distribution of downstream regulatory element antagonist modulator (DREAM) in rat spinal cord and upregulation of its expression during inflammatory pain.下游调节元件拮抗剂调节剂（DREAM）在大鼠脊髓中的分布及其在炎性疼痛期间的表达上调。
Neurochem Res. 2007 Sep;32(9):1592-9. doi: 10.1007/s11064-007-9364-3. Epub 2007 Jun 12.
7
[DREAM: a multifunctional transcriptional regulator].[DREAM：一种多功能转录调节因子]
Sheng Li Xue Bao. 2017 Oct 25;69(5):703-714.
8
Neurotrophins: peripherally and centrally acting modulators of tactile stimulus-induced inflammatory pain hypersensitivity.神经营养因子：触觉刺激诱导的炎性疼痛超敏反应的外周和中枢作用调节剂。
Proc Natl Acad Sci U S A. 1999 Aug 3;96(16):9385-90. doi: 10.1073/pnas.96.16.9385.
9
Brain-derived neurotrophic factor modulates nociceptive sensory inputs and NMDA-evoked responses in the rat spinal cord.脑源性神经营养因子调节大鼠脊髓中的伤害性感觉输入和NMDA诱发的反应。
J Neurosci. 1999 Jun 15;19(12):5138-48. doi: 10.1523/JNEUROSCI.19-12-05138.1999.
10
Increases in mRNA and DREAM protein expression in the rat spinal cord after formalin induced pain.福尔马林诱导疼痛后大鼠脊髓中 mRNA 和 DREAM 蛋白表达增加。
Neurochem Res. 2011 Mar;36(3):533-9. doi: 10.1007/s11064-010-0375-0. Epub 2010 Dec 25.

引用本文的文献

1
Brain-Derived Neurotrophic Factor, Nociception, and Pain.脑源性神经营养因子、伤害感受和疼痛。
Biomolecules. 2024 Apr 30;14(5):539. doi: 10.3390/biom14050539.
2
K Channel-Interacting Proteins in the Neurological and Cardiovascular Systems: An Updated Review.神经系统和心血管系统中的 K 通道相互作用蛋白：最新综述。
Cells. 2023 Jul 20;12(14):1894. doi: 10.3390/cells12141894.
3
Emerging Role of DREAM in Healthy Brain and Neurological Diseases.DRIAM 在健康大脑和神经疾病中的新兴作用。

本文引用的文献

1
The DREAM protein negatively regulates the NMDA receptor through interaction with the NR1 subunit.DREAM 蛋白通过与 NR1 亚基相互作用负调控 NMDA 受体。
J Neurosci. 2010 Jun 2;30(22):7575-86. doi: 10.1523/JNEUROSCI.1312-10.2010.
2
Changes in membrane excitability and potassium currents in sensitized dorsal horn neurons of mice pups.致敏乳鼠背角神经元膜兴奋性和钾电流的变化。
J Neurosci. 2010 Apr 14;30(15):5376-83. doi: 10.1523/JNEUROSCI.4359-09.2010.
3
DREAM (downstream regulatory element antagonist modulator) contributes to synaptic depression and contextual fear memory.
Int J Mol Sci. 2023 May 24;24(11):9177. doi: 10.3390/ijms24119177.
4
IQM-PC332, a Novel DREAM Ligand with Antinociceptive Effect on Peripheral Nerve Injury-Induced Pain.IQM-PC332，一种新型的 DREAM 配体，对周围神经损伤引起的疼痛具有镇痛作用。
Int J Mol Sci. 2022 Feb 15;23(4):2142. doi: 10.3390/ijms23042142.
5
The Circadian Hormone Melatonin Inhibits Morphine-Induced Tolerance and Inflammation via the Activation of Antioxidative Enzymes.昼夜节律激素褪黑素通过激活抗氧化酶抑制吗啡诱导的耐受性和炎症。
Antioxidants (Basel). 2020 Aug 22;9(9):780. doi: 10.3390/antiox9090780.
6
Functional Consequences of Calcium-Dependent Synapse-to-Nucleus Communication: Focus on Transcription-Dependent Metabolic Plasticity.钙依赖性突触-核通讯的功能后果：重点关注依赖转录的代谢可塑性。
Cold Spring Harb Perspect Biol. 2020 Apr 1;12(4):a035287. doi: 10.1101/cshperspect.a035287.
7
Global Gene Knockout of Enhances Pain Sensitivity and Exacerbates Negative Emotions in Rats.基因敲除增强大鼠的疼痛敏感性并加剧其负面情绪。 （注：原文中“Global Gene Knockout of ”后面似乎缺少具体基因名称，此译文是根据大概意思补充完整后翻译的。）
Front Mol Neurosci. 2019 Jan 25;12:5. doi: 10.3389/fnmol.2019.00005. eCollection 2019.
8
KChIP3 N-Terminal 31-50 Fragment Mediates Its Association with TRPV1 and Alleviates Inflammatory Hyperalgesia in Rats.KChIP3 N 端 31-50 片段介导其与 TRPV1 的相互作用并减轻大鼠炎症性痛觉过敏。
J Neurosci. 2018 Feb 14;38(7):1756-1773. doi: 10.1523/JNEUROSCI.2242-17.2018. Epub 2018 Jan 15.
9
Analysis of spontaneous activity of superficial dorsal horn neurons in vitro: neuropathy-induced changes.体外浅层背角神经元自发活动的分析：神经病变引起的变化。
Pflugers Arch. 2016 Nov;468(11-12):2017-2030. doi: 10.1007/s00424-016-1886-6. Epub 2016 Oct 10.
10
Specific cytoarchitectureal changes in hippocampal subareas in daDREAM mice.daDREAM 小鼠海马亚区的特定细胞结构变化。
Mol Brain. 2016 Feb 29;9:22. doi: 10.1186/s13041-016-0204-8.
DREAM（下游调节元件拮抗剂调节剂）有助于突触抑制和情境恐惧记忆。
Mol Brain. 2010 Jan 21;3:3. doi: 10.1186/1756-6606-3-3.
4
The role of calsenilin/DREAM/KChIP3 in contextual fear conditioning.钙调蛋白/DREAM/KChIP3在情境恐惧条件反射中的作用。
Learn Mem. 2009 Feb 17;16(3):167-77. doi: 10.1101/lm.1261709. Print 2009 Mar.
5
Pain facilitation and activity-dependent plasticity in pain modulatory circuitry: role of BDNF-TrkB signaling and NMDA receptors.疼痛调节回路中的疼痛易化与活动依赖性可塑性：脑源性神经营养因子-酪氨酸激酶受体B信号通路和N-甲基-D-天冬氨酸受体的作用
Mol Neurobiol. 2007 Jun;35(3):224-35. doi: 10.1007/s12035-007-0028-8.
6
Long-term potentiation of neuronal excitation by neuron-glia interactions in the rat spinal dorsal horn.大鼠脊髓背角中神经元与神经胶质细胞相互作用对神经元兴奋的长期增强作用。
Eur J Neurosci. 2007 Mar;25(5):1297-306. doi: 10.1111/j.1460-9568.2007.05386.x.
7
Understanding LTP in pain pathways.了解疼痛通路中的长时程增强效应。
Mol Pain. 2007 Apr 3;3:9. doi: 10.1186/1744-8069-3-9.
8
Mouse and rat BDNF gene structure and expression revisited.重新审视小鼠和大鼠脑源性神经营养因子基因的结构与表达。
J Neurosci Res. 2007 Feb 15;85(3):525-35. doi: 10.1002/jnr.21139.
9
Unanticipated region- and cell-specific downregulation of individual KChIP auxiliary subunit isotypes in Kv4.2 knock-out mouse brain.Kv4.2基因敲除小鼠大脑中单个KChIP辅助亚基同种型出现意外的区域和细胞特异性下调。
J Neurosci. 2006 Nov 22;26(47):12137-42. doi: 10.1523/JNEUROSCI.2783-06.2006.
10
The kv4.2 potassium channel subunit is required for pain plasticity.疼痛可塑性需要钾离子通道亚基kv4.2。
Neuron. 2006 Apr 6;50(1):89-100. doi: 10.1016/j.neuron.2006.03.010.