• 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

在使用6-羟基多巴胺治疗导致运动不能的大鼠中,抗胆碱能药物引起的强迫性异常行走。

Compulsive, abnormal walking caused by anticholinergics in akinetic, 6-hydroxydopamine-treated rats.

作者信息

Schallert T, Whishaw I Q, Ramirez V D, Teitelbaum P

出版信息

Science. 1978 Mar 31;199(4336):1461-3. doi: 10.1126/science.564552.

DOI:10.1126/science.564552
PMID:564552
Abstract

In otherwise profoundly akinetic rats that had been severely depleted of brain catecholamines, anticholinergic drugs caused excessive walking. The effect did not appear until 10 days after surgery and then increased with time, suggesting that a phenomenon analogous to denervation supersensitivity may be involved. If the animals walked into corners, they were unable to turn around or back out. Their gait (extremely short steps) was reminiscent of that of patients with Parkinson's disease. The results are consistent with a mutually antagonistic interaction between cholinergic and dopaminergic brain systems and emphasize certain complexities in this interaction.

摘要

在脑儿茶酚胺严重耗竭、原本极度运动不能的大鼠中,抗胆碱能药物会导致过度行走。这种效应直到手术后10天才出现,然后随时间增加,提示可能涉及一种类似于去神经超敏反应的现象。如果动物走到角落里,它们无法转身或退出。它们的步态(步幅极短)让人联想到帕金森病患者的步态。这些结果与胆碱能和多巴胺能脑系统之间相互拮抗的相互作用相一致,并强调了这种相互作用中的某些复杂性。

相似文献

1
Compulsive, abnormal walking caused by anticholinergics in akinetic, 6-hydroxydopamine-treated rats.在使用6-羟基多巴胺治疗导致运动不能的大鼠中,抗胆碱能药物引起的强迫性异常行走。
Science. 1978 Mar 31;199(4336):1461-3. doi: 10.1126/science.564552.
2
Abnormal gait sequence in locomotion after atropine treatment of catecholamine-deficient akinetic rats.对儿茶酚胺缺乏的运动不能大鼠进行阿托品治疗后,其运动中步态序列异常。
Proc Natl Acad Sci U S A. 1987 Dec;84(23):8750-3. doi: 10.1073/pnas.84.23.8750.
3
Muscarinic receptor binding and behavioral effects of atropoine following chronic catecholamine depletion or acetylcholinesterase inhibition in rats.大鼠长期儿茶酚胺耗竭或乙酰胆碱酯酶抑制后阿托品的毒蕈碱受体结合及行为效应
Pharmacol Biochem Behav. 1980 Aug;13(2):187-92. doi: 10.1016/0091-3057(80)90071-4.
4
The effect of anti-Parkinson drugs on catalepsy induced by -methyl-p-tyrosine in rats pretreated with intraventricular 6-hydroxydopamine.抗帕金森病药物对经脑室内注射6-羟基多巴胺预处理的大鼠中由对甲基酪氨酸诱导的僵住症的影响。
Br J Pharmacol. 1973 Mar;47(3):658P-659P.
5
Excessive bracing reactions and their control by atropine and L-DOPA in an animal analog of Parkinsonism.帕金森病动物模型中过度的支撑反应及其由阿托品和左旋多巴进行的控制
Exp Neurol. 1979 Apr;64(1):33-43. doi: 10.1016/0014-4886(79)90003-7.
6
Role of mesencephalic reticular formation in cholinergic-induced catalepsy and anticholinergic reversal of neuroleptic-induced catalepsy.中脑网状结构在胆碱能诱导的僵住症及抗胆碱能药物对神经阻滞剂诱导的僵住症的逆转中的作用。
Brain Res. 1984 Jul 30;307(1-2):47-54. doi: 10.1016/0006-8993(84)90458-x.
7
The effects of 6-hydroxydopamine on vagal cardioaccelerator systems.6-羟基多巴胺对迷走神经心脏加速系统的影响。
J Pharmacol Exp Ther. 1973 Oct;187(1):99-104.
8
[Behavioral changes following lesioning of the nucleus accumbens (ACB) and effects of centrally acting drugs in rats (author's transl)].伏隔核(ACB)损伤后大鼠的行为变化及中枢作用药物的影响(作者译)
Nihon Yakurigaku Zasshi. 1980 May;76(4):227-38.
9
Cardiac catecholamine stores after cardiac sympathectomy, 6-OHDA, and cardiac denervation.心脏交感神经切除术、6-羟基多巴胺处理及心脏去神经支配后心脏儿茶酚胺储备情况
Am J Physiol. 1981 Jun;240(6):H889-95. doi: 10.1152/ajpheart.1981.240.6.H889.
10
Possible behavioural function for noradrenaline--acetylcholine interaction in brain.去甲肾上腺素与乙酰胆碱在大脑中相互作用的潜在行为功能。
Nature. 1979 Feb 1;277(5695):396-6. doi: 10.1038/277396a0.

引用本文的文献

1
Pallidothalamic Circuit-Selective Manipulation Ameliorates Motor Symptoms in a Rat Model of Parkinsonian.苍白球丘脑环路选择性调控改善帕金森病大鼠模型的运动症状。
J Neurosci. 2025 Mar 12;45(11):e0555242025. doi: 10.1523/JNEUROSCI.0555-24.2025.
2
Aerobic exercise improves depressive symptoms in the unilateral 6-OHDA-lesioned rat model of Parkinson's disease.有氧运动可改善帕金森病单侧6-羟基多巴胺损伤大鼠模型的抑郁症状。
IBRO Neurosci Rep. 2024 Mar 12;16:468-475. doi: 10.1016/j.ibneur.2024.03.004. eCollection 2024 Jun.
3
Frequency-Specific Optogenetic Deep Brain Stimulation of Subthalamic Nucleus Improves Parkinsonian Motor Behaviors.
亚深部脑刺激核的频率特异性光遗传学改善帕金森病运动行为。
J Neurosci. 2020 May 27;40(22):4323-4334. doi: 10.1523/JNEUROSCI.3071-19.2020. Epub 2020 Apr 20.
4
Characterization of Motor and Non-Motor Behavioral Alterations in the Dj-1 (PARK7) Knockout Rat.DJ-1(PARK7)基因敲除大鼠的运动和非运动行为改变特征。
J Mol Neurosci. 2019 Oct;69(2):298-311. doi: 10.1007/s12031-019-01358-0. Epub 2019 Jun 27.
5
The acid-sensing ion channel ASIC1a mediates striatal synapse remodeling and procedural motor learning.酸敏离子通道 ASIC1a 介导纹状体突触重塑和程序性运动学习。
Sci Signal. 2018 Aug 7;11(542):eaar4481. doi: 10.1126/scisignal.aar4481.
6
Quantitative Analysis of Catecholamines in the Pink1 -/- Rat Model of Early-onset Parkinson's Disease.在早发性帕金森病的 Pink1 -/- 大鼠模型中儿茶酚胺的定量分析。
Neuroscience. 2018 May 21;379:126-141. doi: 10.1016/j.neuroscience.2018.02.027. Epub 2018 Feb 27.
7
Purinergic Antagonism Prevents Mitochondrial Dysfunction and Behavioral Deficits Associated with Dopaminergic Toxicity Induced by 6-OHDA in Rats.嘌呤能拮抗剂可预防 6-OHDA 诱导的大鼠多巴胺能毒性相关的线粒体功能障碍和行为缺陷。
Neurochem Res. 2017 Dec;42(12):3414-3430. doi: 10.1007/s11064-017-2383-9. Epub 2017 Aug 24.
8
Botulinum Neurotoxin A Injected Ipsilaterally or Contralaterally into the Striatum in the Rat 6-OHDA Model of Unilateral Parkinson's Disease Differently Affects Behavior.在大鼠单侧帕金森病6-OHDA模型中,向纹状体同侧或对侧注射肉毒杆菌神经毒素A对行为的影响不同。
Front Behav Neurosci. 2017 Jun 21;11:119. doi: 10.3389/fnbeh.2017.00119. eCollection 2017.
9
Decomposition of abnormal free locomotor behavior in a rat model of Parkinson's disease.帕金森病大鼠模型中异常自由运动行为的分解。
Front Syst Neurosci. 2013 Nov 27;7:95. doi: 10.3389/fnsys.2013.00095. eCollection 2013.
10
Atp13a2-deficient mice exhibit neuronal ceroid lipofuscinosis, limited α-synuclein accumulation and age-dependent sensorimotor deficits.Atp13a2 缺陷小鼠表现出神经元蜡样脂褐质沉积病,α-突触核蛋白积累有限,以及年龄依赖性感觉运动功能障碍。
Hum Mol Genet. 2013 May 15;22(10):2067-82. doi: 10.1093/hmg/ddt057. Epub 2013 Feb 7.