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抑制P2X7受体可以缓解类似躁狂的行为,而不依赖于白素-1β
Flóra Gölöncsér1, Mária Baranyi1, Pál Tod1
1Laboratory of Molecular Pharmacology, HUN-REN Institute of Experimental Medicine, 1083 Budapest, Hungary.
iScience
|March 6, 2024
概括
purinergic 功能障碍与躁狂有关. 抑制P2X7受体 (P2X7R) 减少了安非他胺诱导的过度活跃,这表明P2X7R,而不是IL-1β,调节了类似躁狂的行为.
科学领域:
- 神经科学是一个神经科学.
- 精神病学是一个精神病学.
- 免疫学 免疫学 免疫学
背景情况:
- 纯能信号传递,特别是通过P2X7受体 (P2X7R),与躁狂和抑郁症等情绪障碍的发病有关.
- 已知P2X7R激活通过NLRP3炎症酶途径调节互白素-1β (IL-1β) 的成熟.
研究的目的:
- 调查P2X7R抑制是否可以缓解亚慢性安非他命 (AMPH) 诱导过活性的小鼠模型中类似躁狂的行为.
- 为了确定任何观察到的行为效应是否通过IL-1β途径进行介导.
主要方法:
- 利用小鼠模型的亚慢性安非他林 (AMPH) 管理来诱导多动性.
- 使用JNJ-47965567,一种选择性P2X7R抗剂,和MCC950,一种NLRP3抑制剂,以评估它们对AMPH诱导行为的影响.
- 测量IL-1β水平,神经递质含量和大脑组织中的多巴胺释放.
- 在野生型 (WT) 和IL-1α/β-Knockout小鼠以及雄性和雌性小鼠中测试了效果.
主要成果:
- P2X7R对抗剂JNJ-47965567在雄性和雌性WT和IL-1α/β淘汰赛小鼠中取消了AMPH诱导的超位运动.
- NLRP3抑制剂MCC950没有减少AMPH诱导的运动,而IL-1受体对抗剂anakinra稍微增加了它.
- AMPH的使用增加了IL-10,TNF-α和TBARS水平,但没有影响BDNF,血清素,多巴胺或诺亚 adrenali 的水平.
- P2X7R对抗和P2rx7基因缺陷,但不是IL-1α/β基因缺陷,减弱AMPH诱导的 [3H]多巴胺从条状切片中的释放.
结论:
- 在小鼠中AMPH诱导的过活性是由P2X7受体调节的.
- P2X7R对AMPH诱导的过活性的调节作用似乎不会通过IL-1β通路进行调节.
- P2X7R对抗是一种潜在的治疗策略,用于躁狂行为,独立于IL-1β信号传递.
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