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利多卡因阻断可卡因线索诱导的记忆再巩固的效果。

The Efficacy of Lidocaine in Disrupting Cocaine Cue-Induced Memory Reconsolidation.

机构信息

Department of Psychiatry, UT Southwestern Medical Center, Dallas, TX USA; School of Behavior and Brain Sciences, UT Dallas, Dallas, TX USA.

Department of Psychiatry, University of Florida, Gainesville, FL USA.

出版信息

Drug Alcohol Depend. 2020 Jul 1;212:108062. doi: 10.1016/j.drugalcdep.2020.108062. Epub 2020 May 12.

Abstract

RATIONAL

Cue-induced craving memories, linked to drug-seeking behaviors, require key molecular processes for memory reconsolidation. Lidocaine, a sodium channel blocker, inhibits NMDA receptor activation and suppresses nitric oxide and ERK production. These processes are required for memory re-consolidation; inhibiting them may reduce cue-related craving memories in cocaine dependent subjects.

OBJECTIVES

To assess the efficacy of lidocaine in decreasing cue-induced cocaine craving and cocaine use.

METHODS

Treatment-seeking cocaine-dependent participants (n = 33, 25 men) were recruited. Personalized craving and relaxation scripts were developed. Participants were then randomly assigned in a double-blind design to either receive intravenous lidocaine immediately following a cocaine craving script (lidocaine/craving), saline following a craving script (saline/craving), or lidocaine following a relaxation script (lidocaine/relax). One week following the infusion, cue-induced craving was assessed in the same paradigm without an infusion. Cocaine use and craving were assessed for 4 weeks following infusion.

RESULTS

The administration of lidocaine during craving induction (lidocaine/craving) did not decrease cue-induced craving during craving reactivation one week later or craving and cocaine use over the 4-week follow-up period compared to the saline/craving group. There were no significant differences in craving and cocaine use between the lidocaine/relax and saline/craving groups.

CONCLUSION

Lidocaine administered following craving induction did not decrease subsequent cue-induced craving or cocaine use. Blocking the reconsolidation of craving-related memories with pharmacological agents remains an important area of investigation.

摘要

理性

与觅药行为相关的线索诱导性渴望记忆需要关键的分子过程来进行记忆再巩固。利多卡因是一种钠离子通道阻滞剂,可抑制 NMDA 受体的激活,并抑制一氧化氮和 ERK 的产生。这些过程是记忆再巩固所必需的;抑制它们可能会减少可卡因依赖受试者与线索相关的渴望记忆。

目的

评估利多卡因降低线索诱导性可卡因渴望和可卡因使用的疗效。

方法

招募了寻求治疗的可卡因依赖参与者(n = 33,25 名男性)。制定了个性化的渴望和放松脚本。然后,参与者以双盲设计随机分为三组:静脉内利多卡因在可卡因渴望脚本后立即给药(利多卡因/渴望)、生理盐水在渴望脚本后给药(生理盐水/渴望)或利多卡因在放松脚本后给药(利多卡因/放松)。在输注后一周,在没有输注的情况下,按照相同的方案评估线索诱导性渴望。在输注后 4 周评估可卡因使用和渴望情况。

结果

在渴望再激活后给予利多卡因(利多卡因/渴望),与生理盐水/渴望组相比,在一周后评估线索诱导性渴望时,或在 4 周随访期间评估渴望和可卡因使用时,并未降低线索诱导性渴望。在利多卡因/放松和生理盐水/渴望组之间,渴望和可卡因使用没有显著差异。

结论

在渴望诱导后给予的利多卡因并未降低随后的线索诱导性渴望或可卡因使用。用药物阻断与渴望相关的记忆的再巩固仍然是一个重要的研究领域。

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