可卡因通过与海马腹侧 D2 受体相互作用,减少雌性大鼠对诱发恐惧记忆的巩固。

IF 3.3 3区 心理学 Q1 BEHAVIORAL SCIENCES
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引用次数: 0

摘要

除了可卡因的成瘾特性外,吸食可卡因还可能导致冒险行为的增加。可卡因对厌恶记忆形成的破坏作用可能是这种行为的基础。本研究采用诱导恐惧条件反射范式研究了可卡因对雌性Sprague Dawley大鼠恐惧记忆的影响,并进一步确定了D2受体在调节可卡因对诱导恐惧表达的影响中的作用。动物接受六次间隔均匀的电击,电击前会发出声音。次日,将大鼠放回恐惧室,在恐惧室中发出声音,但不进行电击。在实验 1 中,可卡因(15 毫克/千克;静注)和 D2 受体拮抗剂依替氯必利(0.1 毫克/千克;静注)在条件反射试验后立即分别或同时给药。结果表明,在巩固期施用可卡因会减少随后测试日的提示恐惧表达。同时服用依替氯必利会减弱这种效应,这表明 D2 受体参与了可卡因对恐惧记忆巩固的有害影响。在实验 2 中,在恐惧条件反射后和施用可卡因前,将依替氯必利(0.05 μg)直接注入腹侧海马(VH)。可卡因继续破坏提示性和情境性恐惧记忆的巩固,而同时在腹侧海马内注射依替氯必利则阻断了这种效应,从而证明 VH D2 受体介导了可卡因诱导的恐惧记忆巩固障碍。总之,本研究提供的证据表明,急性可卡因给药会损害厌恶记忆的形成,并建立了可卡因对恐惧记忆巩固产生有害影响的潜在回路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cocaine diminishes consolidation of cued fear memory in female rats through interactions with ventral hippocampal D2 receptors

In addition to cocaine's addictive properties, cocaine use may lead to heightened risk-taking behavior. The disruptive effects of cocaine on aversive memory formation may underlie this behavior. The present study investigated the effects of cocaine on fear memory using a cued fear conditioning paradigm in female Sprague Dawley rats, and further determined the role of D2 receptors in modulating the effect of cocaine on cued fear expression. Animals received six evenly spaced shocks preceded by a tone. The following day, rats were returned to the fear chamber where tones, but no shocks, were delivered. In Experiment 1, separate or concurrent administrations of cocaine (15 mg/kg; i.p.) and the D2 receptor antagonist eticlopride (0.1 mg/kg; i.p.) were given immediately after conditioning trials. It was determined that cocaine administration during the consolidation period diminished the expression of cued fear during the subsequent test day. Concurrent eticlopride administration attenuated this effect, indicating the involvement of D2 receptors in the deleterious effects of cocaine on fear memory consolidation. In Experiment 2, eticlopride (0.05 μg) was infused directly into the ventral hippocampus (VH) after fear conditioning and before cocaine administration. Cocaine continued to disrupt consolidation of cued and contextual fear memory, and concurrent intra-VH eticlopride blocked this effect, thereby demonstrating that VH D2 receptors mediate cocaine-induced impairment of fear memory consolidation. Overall, the present study provides evidence that acute cocaine administration impairs aversive memory formation and establishes a potential circuit through which cocaine induces its detrimental effects on fear memory consolidation.

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来源期刊
CiteScore
6.40
自引率
2.80%
发文量
122
审稿时长
38 days
期刊介绍: Pharmacology Biochemistry & Behavior publishes original reports in the areas of pharmacology and biochemistry in which the primary emphasis and theoretical context are behavioral. Contributions may involve clinical, preclinical, or basic research. Purely biochemical or toxicology studies will not be published. Papers describing the behavioral effects of novel drugs in models of psychiatric, neurological and cognitive disorders, and central pain must include a positive control unless the paper is on a disease where such a drug is not available yet. Papers focusing on physiological processes (e.g., peripheral pain mechanisms, body temperature regulation, seizure activity) are not accepted as we would like to retain the focus of Pharmacology Biochemistry & Behavior on behavior and its interaction with the biochemistry and neurochemistry of the central nervous system. Papers describing the effects of plant materials are generally not considered, unless the active ingredients are studied, the extraction method is well described, the doses tested are known, and clear and definite experimental evidence on the mechanism of action of the active ingredients is provided.
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