背景:内源性大麻素系统在调节情绪中起着至关重要的作用,但大麻素2型受体(CB2R)在抑郁症中的具体作用仍知之甚少.同样,电针(EA)治疗抑郁症的机制尚不明确.本研究旨在探讨CB2R在抑郁症中的功能,并检查EA的治疗效果是否与海马CB2R系统相关。
方法:使用经历社交失败应激(SDS)的小鼠来模拟抑郁和焦虑行为。我们定量了海马CB2R和N-花生四烯酸乙醇胺(AEA)水平。CB2R激动剂的功效,评估了JWH133在减轻SDS诱导行为方面的作用。此外,评估了EA对CB2R和AEA的影响,以及CB2R拮抗剂AM630对EA抗抑郁作用的影响。
结果:SDS导致抑郁和焦虑样行为,海马CB2R和AEA相应减少。JWH133治疗改善了这些行为。EA治疗导致CB2R和AEA水平升高,而AM630阻断这些抗抑郁作用。
结论:本研究主要集中在SDS模型上,这可能不能完全反映其他抑郁模型。此外,需要进一步研究以了解CB2R和AEA对EA作用的确切机制.
结论:研究表明,海马CB2R和AEA的下调与抑郁症有关。对EA的反应中CB2R和AEA的上调表明它们参与了EA的抗抑郁作用。这些发现为海马CB2R系统在抑郁症中的作用以及EA治疗作用的潜在机制提供了见解。
The endocannabinoid system plays a crucial role in regulating mood, but the specific involvement of cannabinoid receptor type 2 (CB2R) in depression remains poorly understood. Similarly, the mechanisms by which electroacupuncture (EA) provides therapeutic benefits for depression are not clearly defined. This research aims to explore the function of CB2R in depression and examine if the therapeutic effects of EA are associated with the hippocampal CB2R system.
Mice experiencing social defeat stress (SDS) were used to model depression and anxiety behaviors. We quantified hippocampal CB2R and N-arachidonoylethanolamide (
AEA) levels. The efficacy of a CB2R agonist, JWH133, in mitigating SDS-induced behaviors was evaluated. Additionally, EA\'s impact on CB2R and
AEA was assessed, along with the influence of CB2R antagonist AM630 on EA\'s antidepressant effects.
SDS led to depressive and anxiety-like behaviors, with corresponding decreases in hippocampal CB2R and
AEA. Treatment with JWH133 ameliorated these behaviors. EA treatment resulted in increased CB2R and
AEA levels, while AM630 blocked these antidepressant effects.
The study mainly focused on the SDS model, which may not entirely reflect other depression models. Besides, further investigation is needed to understand the precise mechanisms by which CB2R and AEA contribute to EA\'s effects.
The study suggests hippocampal downregulation of CB2R and
AEA contributes to depression. Upregulation of CB2R and AEA in response to EA suggests their involvement in EA\'s antidepressant effects. These findings provide insights into the role of the hippocampal CB2R system in depression and the potential mechanisms underlying EA\'s therapeutic effects.