The endocannabinoid system in anxiety, fear memory and habituation.
The endocannabinoid system in anxiety, fear memory and habituation.
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DOI：
10.1177/0269881111408958
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发表时间：
2012-01
期刊：
影响因子：
--
通讯作者：
Lutz B
中科院分区：
文献类型：
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作者：
Ruehle S;Rey AA;Remmers F;Lutz B
内源性大麻素系统（ECS）参与焦虑和恐惧的证据 积累，为新的治疗方法提供线索。在焦虑中， 已经报道了ECS的双向影响，其中抗焦虑药和致焦虑药 在增加和减少内源性大麻素后都获得了反应 语气最近开发的遗传工具揭示了不同但互补的作用 对GABA能和多巴胺能神经元上大麻素1型（CB 1）受体 人口。这种双重功能，以及CB1受体的可塑性， 表达，特别是在GABA能神经元上，如由应激和奖励诱导的 经验，给予ECS一种独特的调节能力， 体内平衡然而，CB1受体的内源性配体的混杂性 复杂的解释有关ECS和焦虑的实验数据。在恐惧中 在记忆范式中，ECS主要参与两个相反的过程， 重新巩固和消除恐惧记忆。而ECS激活恶化 重新巩固，适当的灭绝取决于完整的CB1受体信号传导。因此， 对于焦虑和恐惧的记忆处理，内源性大麻素信号可能会确保 对压力事件的适当反应。因此，ECS可以被视为 情绪反应的调节缓冲系统。
Evidence for the involvement of the endocannabinoid system (ECS) in anxiety and fear has been accumulated, providing leads for novel therapeutic approaches. In anxiety, a bidirectional influence of the ECS has been reported, whereby anxiolytic and anxiogenic responses have been obtained after both increases and decreases of the endocannabinoid tone. The recently developed genetic tools have revealed different but complementary roles for the cannabinoid type 1 (CB1) receptor on GABAergic and glutamatergic neuronal populations. This dual functionality, together with the plasticity of CB1 receptor expression, particularly on GABAergic neurons, as induced by stressful and rewarding experiences, gives the ECS a unique regulatory capacity for maintaining emotional homeostasis. However, the promiscuity of the endogenous ligands of the CB1 receptor complicates the interpretation of experimental data concerning ECS and anxiety. In fear memory paradigms, the ECS is mostly involved in the two opposing processes of reconsolidation and extinction of the fear memory. Whereas ECS activation deteriorates reconsolidation, proper extinction depends on intact CB1 receptor signalling. Thus, both for anxiety and fear memory processing, endocannabinoid signalling may ensure an appropriate reaction to stressful events. Therefore, the ECS can be considered as a regulatory buffer system for emotional responses.