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卡帕阿片类受体控制了对压力敏感的大脑电路,并驱动寻找可卡因的可卡因

Valentina Martinez Damonte¹, Lydia G Bailey², Amit Thakar²

¹Department of Psychiatry and Behavioral Sciences, Nancy Pritzker Laboratory, Stanford University, Stanford, California 94305.

The Journal of neuroscience : the official journal of the Society for Neuroscience

|September 15, 2025

概括

压力会激活腹部体区域 (VTA) 的卡帕阿片类受体 (kORs),导致人寻找可卡因. 激活kORs在核 (NAc) 输入到VTA上足以恢复寻找毒品的行为.

科学领域:

神经科学是一个神经科学.
成研究研究成研究
分子生物学分子生物学

背景情况:

压力显著触发了在有毒物质使用史的个体中寻找毒品的行为.
卡帕阿片类受体 (kORs) 在调解压力反应方面至关重要.
之前的研究表明,VTA kOR激活阻断了突触可塑性,并恢复了可卡因在压力后寻找.

研究的目的:

为了识别受压力影响的GABAergic输入到VTA.
为了精确确定KOR在VTA中的定位.
为了确定VTA kOR激活是否足以驱动药物恢复.

主要方法:

在小鼠中特定的GABAergic afferents的光遗传激活.
在NAc和多巴胺神经元中有条件的kOR淘汰.
激发性DREADD激活NAc神经元. 激发性DREADD激活NAc神经元. 激发性DREADD激活NAc神经元.
在老鼠中进行kOR激动剂的VTA微注射.

主要成果:

核 (NAc) 到VTA的投射,而不是横向的下丘脑到VTA,显示了对压力敏感的可塑性.
从NAc神经元中删除kOR可以防止压力诱导的可塑性阻断.
激活NAc神经元模仿了压力,阻断了VTA突触的可塑性.
直接的VTA kOR激活恢复了可卡因寻找,而不影响自然的奖励寻找.

结论:

在VTA中的NAc GABAergic终端上的kOR介导了压力诱导的突触可塑性损失.
这种机制有助于压力诱导的成相关行为.
抑制性输入在成电路内的多巴胺神经元兴奋性中起着关键作用.

关键词:

在 LTP LTP 中.它的核心是accumbens的核心.视觉遗传学视觉遗传学塑性的可塑性塑性自主管理的自治.腹部顶部区域的区域.

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