Prefrontal Input to the Periaqueductal Gray Controls Placebo Analgesia

神经科学 导水管周围灰质 扣带回前部 生物神经网络 前额叶皮质 神经化学 安慰剂 岛叶皮质 脑岛 医学 神经网络 吗啡 兴奋性突触后电位 心理学 认知 麻醉 中枢神经系统 抑制性突触后电位 病理 替代医学 中脑
作者
Giulia Livrizzi,Susan T. Lubejko,Desiree A Johnson,Connor Weiss,Janki Patel,Matthew R. Banghart
出处
期刊:The Journal of Pain [Elsevier BV]
卷期号:23 (5): 19-20
标识
DOI:10.1016/j.jpain.2022.03.076
摘要

Placebo analgesia is associated with activity in a highly interconnected neural network distributed throughout the brain. However, this is based on a large body of functional imaging work that primarily relies on correlative measures of neural activity and neurochemical signaling obtained in human subjects, making it challenging to ascribe causal roles to the underlying neural pathways. To address this gap, we developed a mouse model of placebo analgesia and used chemogenetic loss-of-function manipulations to identify the underlying neural circuits. We specifically addressed the role of the descending pain modulatory system (DPMS) and its upstream cortical circuits. We found that chemogenetic inactivation of a subpopulation of excitatory neurons in the ventrolateral periaqueductal gray (vlPAG) abolishes both morphine analgesia and morphine-conditioned placebo analgesia. Placebo, but not morphine analgesia, depends on vlPAG-projecting neurons in the medial prefrontal cortex (mPFC) and anterior cingulate cortex (ACC), but not the anterior insula (AI). For placebo to occur, mPFC-to-vlPAG neurons must be active during conditioning, consistent with a critical role for activity-dependent plasticity in this pathway. Our findings suggest that the vlPAG implements cognitive pain modulation by integrating top-down commands, at least some of which are conveyed directly from the cortex. Grant support from Rita Allen Foundation (non-profit) NIDA grant (R00 DA 034648) Klingenstein-Simons Foundation (non-profit). Placebo analgesia is associated with activity in a highly interconnected neural network distributed throughout the brain. However, this is based on a large body of functional imaging work that primarily relies on correlative measures of neural activity and neurochemical signaling obtained in human subjects, making it challenging to ascribe causal roles to the underlying neural pathways. To address this gap, we developed a mouse model of placebo analgesia and used chemogenetic loss-of-function manipulations to identify the underlying neural circuits. We specifically addressed the role of the descending pain modulatory system (DPMS) and its upstream cortical circuits. We found that chemogenetic inactivation of a subpopulation of excitatory neurons in the ventrolateral periaqueductal gray (vlPAG) abolishes both morphine analgesia and morphine-conditioned placebo analgesia. Placebo, but not morphine analgesia, depends on vlPAG-projecting neurons in the medial prefrontal cortex (mPFC) and anterior cingulate cortex (ACC), but not the anterior insula (AI). For placebo to occur, mPFC-to-vlPAG neurons must be active during conditioning, consistent with a critical role for activity-dependent plasticity in this pathway. Our findings suggest that the vlPAG implements cognitive pain modulation by integrating top-down commands, at least some of which are conveyed directly from the cortex. Grant support from Rita Allen Foundation (non-profit) NIDA grant (R00 DA 034648) Klingenstein-Simons Foundation (non-profit).
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