• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Life sciences >WITHDRAWAL FROM CHRONIC COCAINE ADMINISTRATION CAUSES PROLONGED DEFICITS IN L-TRYPTOPHAN-INDUCED HEAD-TWITCH RESPONSE IN MICE
【24h】

WITHDRAWAL FROM CHRONIC COCAINE ADMINISTRATION CAUSES PROLONGED DEFICITS IN L-TRYPTOPHAN-INDUCED HEAD-TWITCH RESPONSE IN MICE

机译：长期服用可卡因的撤药会导致小鼠L-色氨酸引起的头肌反应的严重缺陷

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Withdrawal from chronic cocaine exposure potentiates the ability of direct 5-HT2A agonists to induce the head-twitch response (HTR) in rodents. This supersensitivity is assumed to be a consequence of cocaine-induced deficits in presynaptic serotonin neurochemistry. The present study utilized the HTR produced by L-tryptophan (TP) to investigate the dose-and time-response effects of cocaine-induced 5-HT deficit. Thus, different groups of mice were injected with cocaine twice daily (0, 0.1, 0.5, 2.5, 5 or 10 mg/kg, i.p.) for 7 or 13 days. During HTR testing procedure, at 24 h after last chronic injection, treated-mice received either: 1) no cocaine; 2) their corresponding daily dose; or 3) a 10 mg/kg dose. In paradigm 1, the frequency of TP-induced HTR was attenuated in a dose-dependent manner in both chronic cocaine regimens. In paradigm 2, small challenge doses (0. 1-2.5 mg/kg) of cocaine in their respective pretreatment groups failed to alter HTR, but larger challenge doses (5 and 10 mg/kg) potentiated the behavior. In paradigm 3, the 10 mg/kg challenge dose potentiated the HTR to a similar degree in both chronically exposed vehicle and various cocaine-treated groups in both treatment regimens. Extended withdrawal studies from cocaine exposure (0, 0.5 and 5 mg/kg twice daily for 7 or 13 days) indicated attenuations in HTR persisted up to 96 h postcocaine abstinence in paradigm 1, whereas paradigm 2 revealed significant attenuations between 48-72 h for 0.5 mg/kg dose; and potentiations for the 5 mg/kg dose persisted throughout the 96 h abstinence. In paradigm 3, no significant effect was observed at 96 h abstinence, but the 10 mg/kg challenge dose significantly potentiated HTR in chronically exposed 10 mg/kg cocaine group 10 days following cocaine abstinence in both exposure regimens. Overall, these results support the notion that chronic cocaine exposure produces prolonged deficits in presynaptic serotonin neurochemistry. Furthermore, serotonergic mechanisms appear to be exquisitely sensitive to chronic administration of both low and high doses of cocaine. [References: 43]
机译：从慢性可卡因暴露中退出可增强直接5-HT2A激动剂在啮齿动物中诱导头抽搐反应（HTR）的能力。这种超敏性被认为是可卡因诱导的突触前5-羟色胺神经化学缺陷的结果。本研究利用L-色氨酸（TP）产生的HTR来研究可卡因诱导的5-HT缺陷的剂量和时间响应效应。因此，向不同组的小鼠每天注射两次可卡因（0、0.1、0.5、2.5、5或10mg / kg，腹腔注射）7天或13天。在HTR测试过程中，最后一次慢性注射后24小时，治疗的小鼠接受以下任何一种治疗：1）没有可卡因; 2）其相应的日剂量;或3）10毫克/公斤的剂量。在范例1中，在两种慢性可卡因方案中，TP诱导的HTR的频率均以剂量依赖性方式减弱。在范例2中，在各自的预处理组中，小剂量的可卡因激发剂量（0-1.2.5 mg / kg）不能改变HTR，但是较大的激发剂量（5和10 mg / kg）增强了行为。在范例3中，在两种治疗方案中，长期暴露的媒介物和各种可卡因治疗组中的10 mg / kg激发剂量均使HTR达到相似的程度。扩大可卡因暴露戒断研究（0、0.5和5 mg / kg每天两次，连续7或13天）表明，范式1的可卡因戒断后HTR的降低持续了96小时，而范式2则显示48-72 h之间的显着降低。 0.5 mg / kg剂量;在整个96小时禁酒期间，5 mg / kg剂量的增强作用持续存在。在范例3中，禁食96 ​​h时未观察到明显的作用，但是在两种暴露方案中，可卡因禁食后10天，长期暴露于10 mg / kg可卡因组的10 mg / kg激发剂量显着增强了HTR。总体而言，这些结果支持以下观点：慢性可卡因暴露会导致突触前5-羟色胺神经化学的长期缺陷。此外，血清素能机制似乎对低剂量和高剂量可卡因的慢性给药极为敏感。 [参考：43]

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号