The identity of cortical circuits mediating nociception and pain is largely unclear. The cingulate cortex is consistently activated during pain, but the functional specificity of cingulate divisions, the roles at distinct temporal phases of central plasticity and the underlying circuitry are unknown. Here we show in mice that the midcingulate division of the cingulate cortex (MCC) does not mediate acute pain sensation and pain affect, but gates sensory hypersensitivity by acting in a wide cortical and subcortical network. Within this complex network, we identified an afferent MCC-posterior insula pathway that can induce and maintain nociceptive hypersensitivity in the absence of conditioned peripheral noxious drive. This facilitation of nociception is brought about by recruitment of descending serotonergic facilitatory projections to the spinal cord. These results have implications for our understanding of neuronal mechanisms facilitating the transition from acute to long-lasting pain.

中文翻译：

---

从中脉皮层到后岛的通路可抑制伤害性超敏反应。

介导伤害感受和疼痛的皮质回路的身份在很大程度上尚不清楚。扣带回皮层在疼痛过程中始终被激活，但是扣带回的功能特异性，中央可塑性在不同时间阶段的作用以及潜在的回路尚不清楚。在这里，我们在小鼠中显示，扣带回皮层（MCC）的中扣带部并不介导急性疼痛感和疼痛影响，而是通过在广泛的皮层和皮层下网络中起作用来控制感觉超敏反应。在这个复杂的网络中，我们确定了传入的MCC-后路岛突路径，可以在没有条件性周围有害驱动的情况下诱导并维持伤害性超敏反应。伤害性感受的这种促进是通过将递减的血清素能促进性突起募集到脊髓而实现的。这些结果对我们理解促进从急性疼痛到持久疼痛的过渡的神经元机制的理解具有启示意义。