Cell的最新研究发现，饥饿可以降低炎性疼痛，但不影响急性疼痛反应。进一步的研究发现，饥饿敏感的AgRP神经元投射到PBN（parabrachial nucleus，臂旁核），抑制炎性疼痛。在饥饿情况下，PBN中的神经肽Y（NPY）-Y1R信号传导降低了炎性疼痛反应（下图）。该研究为慢性疼痛治疗提供了一个新的靶标。
Cell文章摘要：
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.
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