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首页> 外文期刊>Journal of psychopharmacology >Modulation of cannabinoid signaling by hippocampal 5-HT4 serotonergic system in fear conditioning
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Modulation of cannabinoid signaling by hippocampal 5-HT4 serotonergic system in fear conditioning

机译：恐惧调节中海马5-HT4血清素能系统对大麻素信号的调节

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Behavioral studies have suggested a key role for the cannabinoid system in the modulation of conditioned fear memory. Likewise, much of the literature has revealed that the serotonergic system affects Pavlovian fear conditioning and extinction. A high level of functional overlap between the serotonin and cannabinoid systems has also been reported. To clarify the interaction between the hippocampal serotonin (5-HT4) receptor and the cannabinoid CB1 receptor in the acquisition of fear memory, the effects of 5-HT4 agents, arachidonylcyclopropylamide (ACPA; CB1 receptor agonist), and the combined use of these drugs on fear learning were studied in a fear conditioning task in adult male NMRI mice. Pre-training intraperitoneal administration of ACPA (0.1 mg/kg) decreased the percentage of freezing time in both context- and tone-dependent fear conditions, suggesting impairment of the acquisition of fear memory. Pre-training, intra-hippocampal (CA1) microinjection of RS67333, a 5-HT4 receptor agonist, at doses of 0.1 and 0.2 or 0.2 mu g/mouse impaired contextual and tone fear memory, respectively. A subthreshold dose of RS67333 (0.005 mu g/mouse) did not alter the ACPA response in either condition. Moreover, intra-CA1 microinjection of RS23597 as a 5-HT4 receptor antagonist did not alter context-dependent fear memory acquisition, but it did impair tone-dependent fear memory acquisition. However, a subthreshold dose of the RS23597 (0.01 mu g/mouse) potentiated ACPA-induced fear memory impairment in both conditions. Therefore, we suggest that the blockade of hippocampal 5-HT4 serotonergic system modulates cannabinoid signaling induced by the activation of CB1 receptors in conditioned fear.
机译：行为研究表明，大麻素系统在调节条件性恐惧记忆中起关键作用。同样，许多文献都表明，血清素能系统会影响巴甫洛夫恐惧症的消退和灭绝。血清素和大麻素系统之间的功能重叠也很高。为了阐明海马血清素（5-HT4）受体与大麻素CB1受体在恐惧记忆获得中的相互作用，5-HT4药物，花生四烯酸环丙基酰胺（ACPA; CB1受体激动剂）的作用以及这些药物的联合使用在成年雄性NMRI小鼠的恐惧调节任务中研究了关于恐惧学习的知识。训练前腹膜内给予ACPA（0.1 mg / kg）可以降低背景依赖和语气依赖的恐惧条件下的冻结时间百分比，表明恐惧记忆的获得受到损害。训练前的海马内（CA1）微注射RS67333（一种5-HT4受体激动剂）的剂量分别为0.1和0.2或0.2μg/小鼠，削弱了上下文和语气恐惧记忆。亚阈值剂量的RS67333（0.005μg/小鼠）在任何一种情况下均未改变ACPA反应。此外，作为23种5-HT4受体拮抗剂的CA23内CA1显微注射并未改变背景依赖性恐惧记忆的获得，但确实损害了音调依赖性恐惧记忆的获得。但是，亚阈值剂量的RS23597（0.01微克/小鼠）在两种情况下均会增强ACPA诱导的恐惧记忆损害。因此，我们建议在条件恐惧症中，海马5-HT4血清素能系统的阻滞调节由CB1受体的激活诱导的大麻素信号传导。

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