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在腹侧轨道前皮层到背侧条纹体电路中的BDNF适度饮酒,寻求和复发

Sowmya Gunasekaran¹, Jeffrey J Moffat¹, Joshua D Epstein¹

¹Alcohol and Addiction Research Group, Department of Neurology, University of California San Francisco, San Francisco, CA, USA.

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

|November 9, 2025

概括

大脑衍生神经营养因子 (BDNF) 在腹侧轨道前皮层 (vlOFC) 到背侧条纹体 (DLS) 路径中可能会限制酒精摄入. 过度饮酒会破坏这种途径,这表明酒精使用障碍 (AUD) 的治疗目标.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
行为科学行为科学

背景情况:

大脑衍生神经营养因子 (BDNF) 对神经元功能至关重要.
在背侧条纹体 (DLS) 中的BDNF信号保护对抗酒精使用表型.
在DLS中BDNF或其受体TrkB的失调会导致酒精消费升级.

研究的目的:

研究BDNF在腹侧轨道前皮层 (vlOFC) 到DLS电路中的作用,以调节饮酒.
确定大量饮酒是否会破坏这种vLOFC-BDNF通路.
探索增强BDNF信号传递用于酒精使用障碍 (AUD) 的治疗潜力.

主要方法:

鉴定了BDNF阳性神经元从小鼠的vLOFC投射到DLS.
在酒精饮酒和戒断后,评估了 vlOFC 中的 BDNF 表达.
在特定的vLOFC投影途径中操纵的BDNF水平.
使用BDNF受体TrkB激动剂 (LM22A-4) 来评估对寻找酒精的影响.

主要成果:

在酒精循环后,BDNF表达在男性 vlOFC 中下降.
在vLOFC-to-DLS路径中过度表达BDNF减少了酒精摄入量和偏好.
在vLOFC-to-DLS电路中的BDNF减弱了酒精自给,寻求和复发.
TrkB激动剂LM22A-4减少了习惯性寻找酒精的时间.

结论:

在特定的vLOFC-to-DLS神经元组合中的BDNF调节饮酒行为.
由于大量饮酒,这种途径被破坏,导致AUD.
准vLOFC-BDNF-DLS通路为治疗AUD提供了一个潜在的策略.

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