在一项随机对照试验中,通过thalamo-cortical建模捕获的LSD微剂量后长期强化作用的调节
Robin J Murphy1, Kate Godfrey2, Alexander D Shaw3
1School of Pharmacy, University of Auckland, Auckland, New Zealand. robin.murphy@auckland.ac.nz.
BMC neuroscience
|February 5, 2024
概括
微剂量lysergic acid diethylamide (LSD) 没有直接改变视觉长期潜能 (LTP). 然而,动态因果建模揭示了视觉皮层中神经可塑性和层状连接性的变化.
科学领域:
- 神经科学是一个神经科学.
- 心理药理学 心理药理学
背景情况:
- 微剂量迷幻药物,如lysergic acid diethylamide (LSD),据称可以增强认知能力,但缺乏强大的临床测试.
- 临床前研究表明,迷幻药对神经可塑性有影响,可以通过电脑电图 (EEG) 间接评估.
研究的目的:
- 通过视觉长期强化 (LTP) EEG范式,研究微剂量LSD对神经可塑性的急性和累积影响.
- 通过使用动态因果建模 (DCM) 与甲状腺皮层模型 (TCM) 阐明潜在的突触电路变化.
主要方法:
- 健康的成年男性 (n=80) 接受了视觉LTPEEG范式.
- 参与者接受了10微克LSD或安慰剂,急性和6周后每三天进行微剂量治疗.
- 进行了与事件相关的潜在 (ERP) 分析和来源本地化数据的TCM.
主要成果:
- 标准ERP分析显示,视觉诱导的LTP在急性或6周LSD微剂后没有显著变化.
- 甲状腺皮层模型 (TCM) 分析揭示了主要视觉皮层内层状连接的显著变化.
- 急性LSD微剂量影响了自我增益和抑制输入参数,而定期剂量改变了特定皮质层之间的刺激和抑制输入.
结论:
- 传统的ERP峰值分析可能没有足够的灵敏度来检测低剂量LSD的可塑性变化.
- 动态因果建模 (DCM) 为评估神经可塑性提供了更敏感的方法,揭示了可塑性介导层状连接性的差异.
- 这项研究强调了LSD微剂量诱导的潜在突触电路修改,需要进一步调查.
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