可卡因多种药物使用者的中皮层临界功能:关于药物暗示反应性和认知调节的多模式研究
Stephanie G Scala1, Min Su Kang1,2, Sylvia M L Cox3
1Integrated Program in Neuroscience, McGill University, Montreal, Quebec, Canada.
Addiction biology
|January 15, 2024
概括
娱乐性可卡因使用者对药物线索的脑反应加剧. 重复使用可能会降低皮质mGluR5水平,损害渴望调节,增加成的脆弱性.
科学领域:
- 神经科学是一个神经科学.
- 成研究 研究成研究
- 神经成像是一种神经成像.
背景情况:
- 药物成与对药物线索的调节失调的中皮层临床反应有关.
- 改变的谷氨酸传输,特别是甲基增生谷氨酸受体5 (mGluR5),可能会导致成的发展.
- 在成中,mGluR5变化和中皮层临界变化之间的时间和关系尚不清楚.
研究的目的:
- 调查可卡因多种药物使用者的mGluR5水平和中皮层临床变化之间的关系.
- 检查可卡因使用如何影响大脑对药物线索的反应以及调节渴望的能力.
主要方法:
- 使用[11C]ABP688的正子发射断层扫描 (PET) 和功能磁共振成像 (fMRI) 进行.
- 参与者 (可卡因使用者和健康对照组) 观看了与可卡因有关的和中性视频,其中一些试验涉及渴望调节.
- 评估了与可卡因使用史有关的脑活动和mGluR5结合.
主要成果:
- 与对照人群相比,可卡因使用者对药物线索的中皮层临激活增加,特别是在会话的后半部分.
- 认知调节策略降低了可卡因使用者的皮质三角质反应.
- [11C]ABP688结合在整个组之间没有差异,但在暴露于大量可卡因 (≥75次) 的用户中减少.
结论:
- 娱乐性可卡因使用者对可卡因线索表现出偏见的大脑反应.
- 重复使用可卡因可能导致皮质mGluR5水平降低,损害调节药物暗示诱导反应的能力.
- 这些神经生物学变化可能会增加对成的易感性,并建议早期干预的潜在目标.
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