• 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

通过网格试验评估脚桥核损伤大鼠的运动协调障碍及黑质mRNA表达变化

Motor Coordination Disorders Evaluated through the Grid Test and Changes in the Nigral mRNA Expression in Rats with Pedunculopontine Lesion.

作者信息

Lezcano Lisette Blanco, Alberti Amador Esteban, González Fraguela María Elena, Zaldívar Lelo de Larrea Guadalupe, Serrano Rosa Martha Pérez, Jiménez Luna Nadia Angélica, Camejo Rodríguez Dianet, Serrano Sánchez Teresa, Francis Turner Liliana, Estupiñán Díaz Bárbara, Vega Hurtado Yamilé, Fernández Jiménez Isabel

机构信息

Experimental Neurophysiology Department. International Center of Neurological Restoration (CIREN) Ave. 25 No. 15805 e/158 and 160, Playa, Havana 10300, Cuba.

Faculty of Medicine, Autonomous University of Queretaro, Clavel Street No. 200, Col. Prados de la Capilla, Santiago de Querétaro, Querétaro 76176, Mexico.

出版信息

Behav Sci (Basel). 2020 Oct 13;10(10):156. doi: 10.3390/bs10100156.

DOI:10.3390/bs10100156
PMID:33066049
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7600924/
Abstract

UNLABELLED

Neurotoxic lesion of the pedunculopontine nucleus (PPN) is known to cause subtle motor dysfunctions. However, motor coordination during advance on a discontinuous and elevated surface has not been studied. It is also not known whether there are changes in the mRNA expression of nuclear factor (erythroid-derived 2)-like 2 () in nigral tissue.

METHODS

The effects of the unilateral neurotoxic lesion of the PPN in motor coordination evaluated through grid test and mRNA expression in nigral tissue were evaluated. Two experimental designs (ED) were organized: ED#1 behavioral study (7 and 30 days after PPN lesion) and ED#2 molecular biology study (24 h, 48 h and 7 days) after PPN lesion.

RESULTS

ED#1-The number of faults made with left limbs, were significant higher in the lesioned groups ( < 0.01) both 7 and 30 days post-lesion. The number of failures made by the right limbs, was also significantly higher ( < 0.05) vs. control groups. ED#2- mRNA expression showed an increase 24 h after PPN injury ( < 0.01), followed by a peak of expression 48 h post injury ( < 0.001).

CONCLUSIONS

Disorders of motor coordination associated with PPN injury are bilateral. The increased mRNA expression could represent an adaptive response to oxidative stress in the nigral tissue following pontine injury.

摘要

未标记

已知脑桥脚核(PPN)的神经毒性损伤会导致细微的运动功能障碍。然而,在不连续且升高的表面上前进时的运动协调性尚未得到研究。黑质组织中核因子(红系衍生2)样2()的mRNA表达是否存在变化也不清楚。

方法

通过网格试验评估PPN单侧神经毒性损伤对运动协调性的影响,并评估黑质组织中的mRNA表达。组织了两个实验设计(ED):ED#1行为学研究(PPN损伤后7天和30天)和ED#2分子生物学研究(PPN损伤后24小时、48小时和7天)。

结果

ED#1-损伤组左肢出现的错误数量在损伤后7天和30天均显著高于对照组(<0.01)。右肢出现的失误数量与对照组相比也显著更高(<0.05)。ED#2-mRNA表达在PPN损伤后24小时增加(<0.01),随后在损伤后48小时达到表达峰值(<0.001)。

结论

与PPN损伤相关的运动协调性障碍是双侧的。mRNA表达增加可能代表脑桥损伤后黑质组织对氧化应激的适应性反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/9bd217a2d6f5/behavsci-10-00156-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/b0cb3d4342c3/behavsci-10-00156-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/2ab20ea49b24/behavsci-10-00156-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/02fb1fcb35a4/behavsci-10-00156-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/1116555cf504/behavsci-10-00156-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/0a4a0bbf0355/behavsci-10-00156-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/83feb6203c5a/behavsci-10-00156-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/4f58de7cfb48/behavsci-10-00156-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/614058c1e04e/behavsci-10-00156-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/833e54ee0065/behavsci-10-00156-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/9bd217a2d6f5/behavsci-10-00156-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/b0cb3d4342c3/behavsci-10-00156-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/2ab20ea49b24/behavsci-10-00156-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/02fb1fcb35a4/behavsci-10-00156-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/1116555cf504/behavsci-10-00156-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/0a4a0bbf0355/behavsci-10-00156-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/83feb6203c5a/behavsci-10-00156-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/4f58de7cfb48/behavsci-10-00156-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/614058c1e04e/behavsci-10-00156-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/833e54ee0065/behavsci-10-00156-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6b48/7600924/9bd217a2d6f5/behavsci-10-00156-g010.jpg

相似文献

1
Motor Coordination Disorders Evaluated through the Grid Test and Changes in the Nigral mRNA Expression in Rats with Pedunculopontine Lesion.通过网格试验评估脚桥核损伤大鼠的运动协调障碍及黑质mRNA表达变化
Behav Sci (Basel). 2020 Oct 13;10(10):156. doi: 10.3390/bs10100156.
2
Nurr1, Pitx3, and α7 nAChRs mRNA Expression in Nigral Tissue of Rats with Pedunculopontine Neurotoxic Lesion.红核神经元转录因子 1、pituitary homeobox 3 和 α7 烟碱型乙酰胆碱受体 mRNA 在被脑桥被盖部神经毒损伤的大鼠黑质组织中的表达。
Medicina (Kaunas). 2019 Sep 20;55(10):616. doi: 10.3390/medicina55100616.
3
Effect of neurotoxic lesion of pedunculopontine nucleus in nigral and striatal redox balance and motor performance in rats.脚桥核神经毒性损伤对大鼠黑质和纹状体氧化还原平衡及运动能力的影响。
Neuroscience. 2015 Mar 19;289:300-14. doi: 10.1016/j.neuroscience.2014.12.056. Epub 2015 Jan 14.
4
Tyrosine Hydroxylase, Vesicular Monoamine Transporter and Dopamine Transporter mRNA Expression in Nigrostriatal Tissue of Rats with Pedunculopontine Neurotoxic Lesion.脚桥核神经毒性损伤大鼠黑质纹状体组织中酪氨酸羟化酶、囊泡单胺转运体和多巴胺转运体mRNA表达
Behav Sci (Basel). 2018 Feb 1;8(2):20. doi: 10.3390/bs8020020.
5
Motor dysfunction and alterations in glutathione concentration, cholinesterase activity, and BDNF expression in substantia nigra pars compacta in rats with pedunculopontine lesion.脚桥核病变大鼠黑质致密部的运动功能障碍以及谷胱甘肽浓度、胆碱酯酶活性和脑源性神经营养因子表达的改变。
Neuroscience. 2017 Apr 21;348:83-97. doi: 10.1016/j.neuroscience.2017.02.008. Epub 2017 Feb 15.
6
Temporal-Spatial Profiling of Pedunculopontine Galanin-Cholinergic Neurons in the Lactacystin Rat Model of Parkinson's Disease.帕金森病乳斑硷乙酰转移酶大鼠模型中脑桥被盖腹侧区微量注射亮氨酸脑啡肽神经元的时空分析。
Neurotox Res. 2018 Jul;34(1):16-31. doi: 10.1007/s12640-017-9846-2. Epub 2017 Dec 7.
7
Role of pedunculopontine cholinergic neurons in the vulnerability of nigral dopaminergic neurons in Parkinson's disease.脑桥被盖部胆碱能神经元在帕金森病中黑质多巴胺能神经元易损性中的作用。
Exp Neurol. 2016 Jan;275 Pt 1:209-19. doi: 10.1016/j.expneurol.2015.11.004. Epub 2015 Nov 10.
8
[Reduction of apomorphine-induced rotation in rats with additional destruction of the pedunculopontine nucleus contralateral to the unilateral nigrostriatal lesion].
No To Shinkei. 1998 Jan;50(1):33-7.
9
High-frequency stimulation of the subthalamic nucleus modulates the activity of pedunculopontine neurons through direct activation of excitatory fibres as well as through indirect activation of inhibitory pallidal fibres in the rat.高频刺激丘脑底核可通过直接激活兴奋性纤维以及间接激活大鼠苍白球抑制性纤维来调节脚桥核神经元的活动。
Eur J Neurosci. 2007 Feb;25(4):1174-86. doi: 10.1111/j.1460-9568.2007.05360.x.
10
Unilateral lesion of the pedunculopontine nucleus induces hyperactivity in the subthalamic nucleus and substantia nigra in the rat.脚桥核单侧损伤会诱发大鼠丘脑底核和黑质的活动亢进。
Eur J Neurosci. 2005 Nov;22(9):2283-94. doi: 10.1111/j.1460-9568.2005.04402.x.

引用本文的文献

1
NeuroAiD-II (MLC901) Promoted Neurogenesis by Activating the PI3K/AKT/GSK-3β Signaling Pathway in Rat Spinal Cord Injury Models.在大鼠脊髓损伤模型中,NeuroAiD-II(MLC901)通过激活PI3K/AKT/GSK-3β信号通路促进神经发生。
Biomedicines. 2024 Aug 21;12(8):1920. doi: 10.3390/biomedicines12081920.

本文引用的文献

1
Nurr1, Pitx3, and α7 nAChRs mRNA Expression in Nigral Tissue of Rats with Pedunculopontine Neurotoxic Lesion.红核神经元转录因子 1、pituitary homeobox 3 和 α7 烟碱型乙酰胆碱受体 mRNA 在被脑桥被盖部神经毒损伤的大鼠黑质组织中的表达。
Medicina (Kaunas). 2019 Sep 20;55(10):616. doi: 10.3390/medicina55100616.
2
Activators and Inhibitors of NRF2: A Review of Their Potential for Clinical Development.NRF2 的激活剂和抑制剂:临床开发潜力的综述。
Oxid Med Cell Longev. 2019 Jul 14;2019:9372182. doi: 10.1155/2019/9372182. eCollection 2019.
3
Pharmacoepigenomic Interventions as Novel Potential Treatments for Alzheimer's and Parkinson's Diseases.
药物基因组干预作为阿尔茨海默病和帕金森病的新型潜在治疗方法。
Int J Mol Sci. 2018 Oct 16;19(10):3199. doi: 10.3390/ijms19103199.
4
On Cell Loss and Selective Vulnerability of Neuronal Populations in Parkinson's Disease.帕金森病中神经元群体的细胞丢失与选择性易损性
Front Neurol. 2018 Jun 19;9:455. doi: 10.3389/fneur.2018.00455. eCollection 2018.
5
A Review of the Pedunculopontine Nucleus in Parkinson's Disease.帕金森病中脚桥核的综述
Front Aging Neurosci. 2018 Apr 26;10:99. doi: 10.3389/fnagi.2018.00099. eCollection 2018.
6
Tyrosine Hydroxylase, Vesicular Monoamine Transporter and Dopamine Transporter mRNA Expression in Nigrostriatal Tissue of Rats with Pedunculopontine Neurotoxic Lesion.脚桥核神经毒性损伤大鼠黑质纹状体组织中酪氨酸羟化酶、囊泡单胺转运体和多巴胺转运体mRNA表达
Behav Sci (Basel). 2018 Feb 1;8(2):20. doi: 10.3390/bs8020020.
7
The role of Nrf2 signaling in counteracting neurodegenerative diseases.Nrf2 信号通路在对抗神经退行性疾病中的作用。
FEBS J. 2018 Oct;285(19):3576-3590. doi: 10.1111/febs.14379. Epub 2018 Jan 29.
8
Dopamine and Acetylcholine, a Circuit Point of View in Parkinson's Disease.多巴胺与乙酰胆碱:帕金森病的一个环路观点。
Front Neural Circuits. 2017 Dec 22;11:110. doi: 10.3389/fncir.2017.00110. eCollection 2017.
9
Nrf2, the Master Regulator of Anti-Oxidative Responses.Nrf2,抗氧化反应的主要调节因子。
Int J Mol Sci. 2017 Dec 20;18(12):2772. doi: 10.3390/ijms18122772.
10
Motor dysfunction and alterations in glutathione concentration, cholinesterase activity, and BDNF expression in substantia nigra pars compacta in rats with pedunculopontine lesion.脚桥核病变大鼠黑质致密部的运动功能障碍以及谷胱甘肽浓度、胆碱酯酶活性和脑源性神经营养因子表达的改变。
Neuroscience. 2017 Apr 21;348:83-97. doi: 10.1016/j.neuroscience.2017.02.008. Epub 2017 Feb 15.