一种用于抑制竞争需求状态引起的疼痛的神经回路。
A Neural Circuit for the Suppression of Pain by a Competing Need State.
机构信息
Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA.
Department of Biobehavioral Health Sciences, University of Pennsylvania, Philadelphia, PA 19104, USA.
出版信息
Cell. 2018 Mar 22;173(1):140-152.e15. doi: 10.1016/j.cell.2018.02.057.
Hunger and pain are two competing signals that individuals must resolve to ensure survival. However, the neural processes that prioritize conflicting survival needs are poorly understood. We discovered that hunger attenuates behavioral responses and affective properties of inflammatory pain without altering acute nociceptive responses. This effect is centrally controlled, as activity in hunger-sensitive agouti-related protein (AgRP)-expressing neurons abrogates inflammatory pain. Systematic analysis of AgRP projection subpopulations revealed that the neural processing of hunger and inflammatory pain converge in the hindbrain parabrachial nucleus (PBN). Strikingly, activity in AgRP → PBN neurons blocked the behavioral response to inflammatory pain as effectively as hunger or analgesics. The anti-nociceptive effect of hunger is mediated by neuropeptide Y (NPY) signaling in the PBN. By investigating the intersection between hunger and pain, we have identified a neural circuit that mediates competing survival needs and uncovered NPY Y1 receptor signaling in the PBN as a target for pain suppression.
饥饿和疼痛是个体必须解决以确保生存的两种相互竞争的信号。然而，优先考虑冲突性生存需求的神经过程还知之甚少。我们发现，饥饿会减弱炎症性疼痛的行为反应和情感属性，而不会改变急性伤害性反应。这种效应是中枢控制的，因为饥饿敏感的 agouti 相关蛋白（AgRP）表达神经元的活动消除了炎症性疼痛。对 AgRP 投射亚群的系统分析表明，饥饿和炎症性疼痛的神经处理在脑桥臂旁核（PBN）中汇聚。引人注目的是，AgRP→PBN 神经元的活动阻断炎症性疼痛的行为反应的效果与饥饿或镇痛药一样有效。饥饿的抗伤害作用是通过 PBN 中的神经肽 Y（NPY）信号介导的。通过研究饥饿和疼痛之间的交集，我们确定了介导竞争生存需求的神经回路，并发现 PBN 中的 NPY Y1 受体信号作为抑制疼痛的靶点。
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