• 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

相似文献

1
Cocaine Exposure Results in Formation of Dendritic Varicosity in Rat Primary Hippocampal Neurons.可卡因暴露导致大鼠原代海马神经元形成树突膨体。
Am J Infect Dis. 2009 Jan 1;5(1):26-30. doi: 10.3844/ajidsp.2009.26.30.
2
Cocaine and human immunodeficiency virus type 1 gp120 mediate neurotoxicity through overlapping signaling pathways.可卡因和人类免疫缺陷病毒1型糖蛋白120通过重叠的信号通路介导神经毒性。
J Neurovirol. 2009 Apr;15(2):164-75. doi: 10.1080/13550280902755375.
3
Mechanisms of Platelet-Derived Growth Factor-BB in Restoring HIV Tat-Cocaine-Mediated Impairment of Neuronal Differentiation.血小板衍生生长因子-BB恢复HIV反式激活蛋白-可卡因介导的神经元分化损伤的机制
Mol Neurobiol. 2016 Nov;53(9):6377-6387. doi: 10.1007/s12035-015-9536-0. Epub 2015 Nov 17.
4
HIV-1 Tat induced microglial EVs leads to neuronal synaptodendritic injury: microglia-neuron cross-talk in NeuroHIV.HIV-1反式激活因子诱导的小胶质细胞细胞外囊泡导致神经元突触树突损伤:神经艾滋病中的小胶质细胞-神经元相互作用。
Extracell Vesicles Circ Nucl Acids. 2022;3(2):133-149. doi: 10.20517/evcna.2022.14. Epub 2022 May 31.
5
Dysregulation of Neuronal Cholesterol Homeostasis upon Exposure to HIV-1 Tat and Cocaine Revealed by RNA-Sequencing.暴露于 HIV-1 Tat 和可卡因下神经元胆固醇稳态的失调可通过 RNA 测序揭示。
Sci Rep. 2018 Nov 2;8(1):16300. doi: 10.1038/s41598-018-34539-9.
6
Cocaine potentiates astrocyte toxicity mediated by human immunodeficiency virus (HIV-1) protein gp120.可卡因增强了人类免疫缺陷病毒(HIV-1)蛋白 gp120 介导的星形胶质细胞毒性。
PLoS One. 2010 Oct 15;5(10):e13427. doi: 10.1371/journal.pone.0013427.
7
Network analysis of hippocampal neurons by microelectrode array in the presence of HIV-1 Tat and cocaine.在 HIV-1 Tat 和可卡因存在的情况下通过微电极阵列分析海马神经元的网络。
J Cell Physiol. 2018 Dec;233(12):9299-9311. doi: 10.1002/jcp.26322. Epub 2018 Jun 22.
8
Cocaine-mediated enhancement of Tat toxicity in rat hippocampal cell cultures: the role of oxidative stress and D1 dopamine receptor.可卡因介导的大鼠海马细胞培养物中Tat毒性增强:氧化应激和D1多巴胺受体的作用
Neurotoxicology. 2006 Mar;27(2):217-28. doi: 10.1016/j.neuro.2005.10.003. Epub 2005 Dec 28.
9
Methamphetamine augments HIV-1 gp120 inhibition of synaptic transmission and plasticity in rat hippocampal slices: Implications for methamphetamine exacerbation of HIV-associated neurocognitive disorders.甲基苯丙胺增强 HIV-1 gp120 抑制大鼠海马切片中的突触传递和可塑性:提示甲基苯丙胺加剧与 HIV 相关的神经认知障碍。
Neurobiol Dis. 2022 Jun 15;168:105712. doi: 10.1016/j.nbd.2022.105712. Epub 2022 Mar 22.
10
Osteopontin and Integrin Mediated Modulation of Post-Synapses in HIV Envelope Glycoprotein Exposed Hippocampal Neurons.骨桥蛋白和整合素介导的HIV包膜糖蛋白暴露的海马神经元突触后调节
Brain Sci. 2020 Jun 4;10(6):346. doi: 10.3390/brainsci10060346.

引用本文的文献

1
Crossroads of Drug Abuse and HIV Infection: Neurotoxicity and CNS Reservoir.药物滥用与艾滋病毒感染的交叉点:神经毒性与中枢神经系统储存库
Vaccines (Basel). 2022 Jan 27;10(2):202. doi: 10.3390/vaccines10020202.
2
Cocaine-mediated activation of microglia and microglial MeCP2 and BDNF production.可卡因介导的小胶质细胞激活和小胶质细胞 MeCP2 和 BDNF 的产生。
Neurobiol Dis. 2018 Sep;117:28-41. doi: 10.1016/j.nbd.2018.05.017. Epub 2018 May 30.
3
Cocaine-mediated induction of microglial activation involves the ER stress-TLR2 axis.可卡因介导的小胶质细胞激活涉及内质网应激-TLR2轴。
J Neuroinflammation. 2016 Feb 9;13:33. doi: 10.1186/s12974-016-0501-2.
4
Drugs of Abuse in HIV infection and neurotoxicity.HIV感染中的滥用药物与神经毒性
Front Microbiol. 2015 Mar 24;6:217. doi: 10.3389/fmicb.2015.00217. eCollection 2015.
5
Cocaine induces nuclear export and degradation of neuronal retinoid X receptor-γ via a TNF-α/JNK- mediated mechanism.可卡因通过肿瘤坏死因子-α/应激活化蛋白激酶介导的机制诱导神经元维甲酸X受体-γ的核输出和降解。
J Neuroimmune Pharmacol. 2015 Mar;10(1):55-73. doi: 10.1007/s11481-014-9573-x. Epub 2015 Jan 14.
6
Role of endoplasmic reticulum (ER) stress in cocaine-induced microglial cell death.内质网应激在可卡因诱导的小胶质细胞死亡中的作用。
J Neuroimmune Pharmacol. 2013 Jun;8(3):705-14. doi: 10.1007/s11481-013-9438-8. Epub 2013 Feb 13.
7
Cocaine and HIV-1 interplay: molecular mechanisms of action and addiction.可卡因与 HIV-1 的相互作用:作用机制和成瘾的分子基础。
J Neuroimmune Pharmacol. 2011 Dec;6(4):503-15. doi: 10.1007/s11481-011-9297-0. Epub 2011 Jul 16.

本文引用的文献

1
Acute cocaine exposure alters spine density and long-term potentiation in the ventral tegmental area.急性可卡因暴露会改变腹侧被盖区的树突棘密度和长时程增强效应。
Eur J Neurosci. 2007 Aug;26(3):749-56. doi: 10.1111/j.1460-9568.2007.05689.x.
2
Cocaine exposure in vitro induces apoptosis in fetal locus coeruleus neurons through TNF-alpha-mediated induction of Bax and phosphorylated c-Jun NH(2)-terminal kinase.体外可卡因暴露通过肿瘤坏死因子-α介导的Bax诱导和磷酸化c-Jun氨基末端激酶诱导胎儿蓝斑神经元凋亡。
J Neurochem. 2007 Oct;103(2):542-56. doi: 10.1111/j.1471-4159.2007.04750.x. Epub 2007 Jul 17.
3
Corticostriatal up-regulation of activity-regulated cytoskeletal-associated protein expression after repeated exposure to cocaine.反复接触可卡因后皮质纹状体中活性调节细胞骨架相关蛋白表达的上调。
Mol Pharmacol. 2006 Nov;70(5):1726-34. doi: 10.1124/mol.106.026302. Epub 2006 Aug 14.
4
Specificity of prenatal cocaine on inhibition of locus coeruleus neurite outgrowth.产前可卡因对蓝斑神经突生长抑制的特异性。
Neuroscience. 2006;139(3):899-907. doi: 10.1016/j.neuroscience.2005.12.053. Epub 2006 Feb 17.
5
Cocaine-mediated enhancement of Tat toxicity in rat hippocampal cell cultures: the role of oxidative stress and D1 dopamine receptor.可卡因介导的大鼠海马细胞培养物中Tat毒性增强:氧化应激和D1多巴胺受体的作用
Neurotoxicology. 2006 Mar;27(2):217-28. doi: 10.1016/j.neuro.2005.10.003. Epub 2005 Dec 28.
6
Synaptic activity becomes excitotoxic in neurons exposed to elevated levels of platelet-activating factor.在暴露于高水平血小板活化因子的神经元中,突触活动会变得具有兴奋性毒性。
J Clin Invest. 2005 Nov;115(11):3185-92. doi: 10.1172/JCI25444.
7
Long-term potentiation in the rat dentate gyrus is associated with enhanced Arc/Arg3.1 protein expression in spines, dendrites and glia.大鼠齿状回中的长时程增强与棘突、树突和胶质细胞中Arc/Arg3.1蛋白表达增强相关。
Eur J Neurosci. 2005 May;21(9):2384-96. doi: 10.1111/j.1460-9568.2005.04068.x.
8
Dendritic spines lost during glutamate receptor activation reemerge at original sites of synaptic contact.在谷氨酸受体激活过程中丢失的树突棘会在突触接触的原始部位重新出现。
J Neurosci. 2001 Apr 1;21(7):2393-403. doi: 10.1523/JNEUROSCI.21-07-02393.2001.
9
Estrogen protects against the synergistic toxicity by HIV proteins, methamphetamine and cocaine.雌激素可抵御由艾滋病毒蛋白、甲基苯丙胺和可卡因造成的协同毒性。
BMC Neurosci. 2001;2:3. doi: 10.1186/1471-2202-2-3. Epub 2001 Mar 2.
10
Synergistic neurotoxicity of opioids and human immunodeficiency virus-1 Tat protein in striatal neurons in vitro.阿片类药物与人类免疫缺陷病毒1型Tat蛋白在体外对纹状体神经元的协同神经毒性作用
Neuroscience. 2001;102(3):555-63. doi: 10.1016/s0306-4522(00)00461-9.

可卡因暴露导致大鼠原代海马神经元形成树突膨体。

Cocaine Exposure Results in Formation of Dendritic Varicosity in Rat Primary Hippocampal Neurons.

作者信息

Yao Honghong, Bethel-Brown Crystal, Buch Shilpa

机构信息

Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160.

出版信息

Am J Infect Dis. 2009 Jan 1;5(1):26-30. doi: 10.3844/ajidsp.2009.26.30.

DOI:10.3844/ajidsp.2009.26.30
PMID:20046918
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2749690/
Abstract

While it has been well documented that drugs of abuse such as cocaine can cause enhanced progression of HIV-Associated Neuropathological Disorders (HAND), the underlying mechanisms mediating these effects remain poorly understood. In the present study, we explored the impact of cocaine exposure (I μM and 10 μM) on the dendritic beading in rat primary hippocampal neurons. Using the approach of transfection with green fluorescent protein, we observed significant dendritic swelling in hippocampal neurons exposed to 10 μM but not 1 μM of cocaine when compared with the saline treated group. Cocaine exposure also resulted in decreased expression of the synaptic plasticity gene, Arc as evidenced by Western blotting. Intriguingly, cocaine exposure of primary neurons in the presence of the neurotoxin-HIV envelope protein gp 120, resulted in increased enhancement of neuronal beading as compared with exposure of neurons to either agent alone. Taken together these findings imply that cocaine in co-operation with HIV protein exacerbates neuronal damage in the brains of HIV-infected cocaine abusers.

摘要

虽然已有充分文献记载,可卡因等滥用药物会导致与HIV相关的神经病理障碍(HAND)病情加速发展,但其介导这些效应的潜在机制仍知之甚少。在本研究中,我们探究了可卡因暴露(1 μM和10 μM)对大鼠原代海马神经元树突串珠形成的影响。采用绿色荧光蛋白转染方法,我们观察到,与生理盐水处理组相比,暴露于10 μM而非1 μM可卡因的海马神经元出现了明显的树突肿胀。蛋白质印迹法证实,可卡因暴露还导致突触可塑性基因Arc的表达降低。有趣的是,与单独将神经元暴露于任一药物相比,在存在神经毒素HIV包膜蛋白gp 120的情况下,原代神经元暴露于可卡因会导致神经元串珠形成增强。综合这些发现表明,可卡因与HIV蛋白协同作用会加剧HIV感染的可卡因滥用者大脑中的神经元损伤。