• 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

三碘甲状腺原氨酸增强抗抑郁药诱导的大鼠习得性无助逆转作用。

Triiodothyronine potentiation of antidepressant-induced reversal of learned helplessness in rats.

作者信息

Brochet D M, Martin P, Soubrié P, Simon P

出版信息

Psychiatry Res. 1987 Jul;21(3):267-75. doi: 10.1016/0165-1781(87)90031-x.

DOI:10.1016/0165-1781(87)90031-x
PMID:3628611
Abstract

Several clinical investigations have suggested that a special relationship exists between thyroid function and affective disorders and/or therapeutic response to antidepressants. The present report describes that the reversal by antidepressants (imipramine, desipramine, and nomifensine) of depressive-like behavior in rats (escape deficits produced by previous exposure to uncontrollable stress) was significantly hastened in animals given daily triiodothyronine (T3). The learned helplessness paradigm might be a useful model for approaching in animals the neurohormonal correlates of affective disorders and the neurobiochemical bases of the reported T3 enhancement of antidepressants.

摘要

多项临床研究表明,甲状腺功能与情感障碍和/或对抗抑郁药的治疗反应之间存在特殊关系。本报告描述了在每日给予三碘甲状腺原氨酸(T3)的动物中,抗抑郁药(丙咪嗪、地昔帕明和诺米芬辛)对大鼠抑郁样行为(先前暴露于不可控应激所产生的逃避缺陷)的逆转作用显著加快。习得性无助范式可能是一种有用的模型,可用于在动物中探讨情感障碍的神经激素相关性以及所报道的T3增强抗抑郁药作用的神经生化基础。

相似文献

1
Triiodothyronine potentiation of antidepressant-induced reversal of learned helplessness in rats.三碘甲状腺原氨酸增强抗抑郁药诱导的大鼠习得性无助逆转作用。
Psychiatry Res. 1987 Jul;21(3):267-75. doi: 10.1016/0165-1781(87)90031-x.
2
Triiodothyroacetic acid (TRIAC) potentiation of antidepressant-induced reversal of learned helplessness in rats.三碘甲状腺乙酸(TRIAC)增强抗抑郁药诱导的大鼠习得性无助逆转作用。
Eur J Pharmacol. 1988 Aug 2;152(3):347-51. doi: 10.1016/0014-2999(88)90730-3.
3
The reversal effect of antidepressants on the escape deficit induced by inescapable shock in rats.抗抑郁药对大鼠不可逃避电击所致逃避缺陷的逆转作用。
Psychopharmacology (Berl). 1983;80(3):206-8. doi: 10.1007/BF00436153.
4
Thyroid function and reversal by antidepressant drugs of depressive-like behavior (escape deficits) in rats.甲状腺功能以及抗抑郁药物对大鼠抑郁样行为(逃避缺陷)的逆转作用。
Neuropsychobiology. 1987;18(1):21-6. doi: 10.1159/000118388.
5
Helpless behavior (escape deficits) in streptozotocin-diabetic rats: resistance to antidepressant drugs.链脲佐菌素诱导的糖尿病大鼠的无助行为(逃避缺陷):对抗抑郁药物的抵抗性
Psychoneuroendocrinology. 1989;14(1-2):145-53. doi: 10.1016/0306-4530(89)90064-4.
6
Tricyclic antidepressants, thyroid function, and their relationship with the behavioral responses in rats.三环类抗抑郁药、甲状腺功能及其与大鼠行为反应的关系。
Biol Psychiatry. 1990 Dec 1;28(11):967-78. doi: 10.1016/0006-3223(90)90062-7.
7
Triiodothyroacetic acid-induced reversal of learned helplessness in rats.三碘甲状腺乙酸诱导大鼠习得性无助的逆转。
Eur J Pharmacol. 1987 Feb 24;134(3):345-8. doi: 10.1016/0014-2999(87)90367-0.
8
Captopril as an antidepressant? Effects on the learned helplessness paradigm in rats.
Biol Psychiatry. 1990 May 1;27(9):968-74. doi: 10.1016/0006-3223(90)90034-y.
9
Decreased GABA B receptors in helpless rats: reversal by tricyclic antidepressants.无助大鼠中γ-氨基丁酸B受体减少:三环类抗抑郁药的逆转作用。
Neuropsychobiology. 1989;22(4):220-4. doi: 10.1159/000118620.
10
Effects of rolipram, a phosphodiesterase 4 inhibitor, in combination with imipramine on depressive behavior, CRE-binding activity and BDNF level in learned helplessness rats.磷酸二酯酶4抑制剂咯利普兰与丙咪嗪联用对习得性无助大鼠抑郁行为、CRE结合活性及脑源性神经营养因子水平的影响
Eur J Pharmacol. 2004 Sep 13;498(1-3):135-42. doi: 10.1016/j.ejphar.2004.07.084.

引用本文的文献

1
Mechanisms of antidepressant resistance.抗抑郁药耐药性的机制。
Front Pharmacol. 2013 Nov 22;4:146. doi: 10.3389/fphar.2013.00146.
2
Effect of controllable stress on myosin heavy chain expression and muscle-specific protection by clomipramine.可控应激对肌球蛋白重链表达的影响以及氯米帕明对肌肉的特异性保护作用。
J Muscle Res Cell Motil. 1998 Oct;19(7):803-10. doi: 10.1023/a:1005407621894.