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首页> 外文期刊>Neurobiology of learning and memory >Pre-training anandamide infusion within the basolateral amygdala impairs plus-maze discriminative avoidance task in rats.
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Pre-training anandamide infusion within the basolateral amygdala impairs plus-maze discriminative avoidance task in rats.

机译：训练前的杏仁核基底外侧输注anandamide会损害大鼠的迷宫判别性规避任务。

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摘要

Endocannabinoids (eCBs) modulate a variety of brain functions via activation of the widely expressed CB1 receptor. One site of high density of this receptor is the basolateral amygdala (BLA), a structure involved in the formation of aversive memories. The activation and blockade of CB1 receptors by systemic or hippocampal drug administrations have been shown to modify memory processing. However, little is known about the role of the BLA endocannabinoid system in aversive memories. Additionally, BLA endocannabinoid transmission seems to be related to emotional states, but the relevance of these effects to memory formation is still unknown. In this study we investigated the effects of the eCB anandamide (AEA) and the CB1 antagonist/inverse agonist AM251 infused into the BLA on the acquisition of an aversive memory task, concomitantly evaluating basal anxiety levels in rats. Male rats received pre-training micro-injection of AEA, AM251 or vehicle bilaterally into the BLA, and were studied with the plus-maze discriminative avoidance task (a paradigm that allows concomitant and independent evaluation of anxiety-like behavior and the memory of an aversive task). Our results showed that AEA into the BLA before training prevented memory retrieval 24 h later, as evaluated by exploration of the aversive arm of the maze, while AM251 into the BLA did not interfere with animals' performance. In addition, AEA had no effect on anxiety-like behavior (as evaluated by open arm exploration and risk assessment), while AM251 induced an anxiogenic effect. Our data indicate an important role of BLA CB1 receptors in aversive memory formation, and suggest that this involvement is not necessarily related to a possible modulation of anxiety states.
机译：内源性大麻素（eCBs）通过激活广泛表达的CB1受体来调节多种脑功能。该受体高密度的一个位点是基底外侧杏仁核（BLA），该结构与厌恶记忆的形成有关。通过全身性或海马性药物给药，CB1受体的激活和阻断已显示出可以改变记忆过程。但是，关于厌恶性记忆中BLA内源性大麻素系统的作用知之甚少。此外，BLA内源性大麻素的传递似乎与情绪状态有关，但这些作用与记忆形成的相关性仍未知。在这项研究中，我们调查了eCB anandamide（AEA）和注入BLA的CB1拮抗剂/反向激动剂AM251对厌恶性记忆任务的获取，并同时评估了大鼠的基础焦虑水平。雄性大鼠接受双侧ALA，AM251或媒介物的预训练性双侧注射到BLA中，并进行了正迷宫判别性规避任务（该范式可以同时独立评估焦虑样行为和记忆令人反感的任务）。我们的结果表明，通过探索迷宫的厌恶臂评估，训练前进入BLA的AEA阻止了24小时后的记忆恢复，而进入BLA的AM251不会干扰动物的行为。此外，AEA对焦虑样行为没有影响（通过开臂探查和风险评估进行评估），而AM251则具有焦虑作用。我们的数据表明BLA CB1受体在厌恶记忆形成中的重要作用，并表明这种参与并不一定与焦虑状态的可能调节有关。

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