Uddin Olivia, Studlack Paige, Akintola Titilola, Raver Charles, Castro Alberto, Masri Radi, Keller Asaf
Department of Anatomy and Neurobiology, University of Maryland School of Medicine, 20 Penn St, HSF-II S251, Baltimore, MD 21201, United States.
Program in Neuroscience, University of Maryland School of Medicine, 20 Penn St, HSF-II S251, Baltimore, MD 21201, United States.
Neurobiol Pain. 2018 Jan-Jul;3:22-30. doi: 10.1016/j.ynpai.2018.02.002. Epub 2018 Mar 1.
The parabrachial (PB) complex mediates both ascending nociceptive signaling and descending pain modulatory information in the affective/emotional pain pathway. We hypothesized that PB hyperactivity influences chronic pain behavior after trigeminal nerve injury in rats. Following induction of neuropathic pain using the chronic constriction injury of the infraorbital nerve (CCI-ION) model, rats displayed spontaneous markers of pain and mechanical hyperalgesia extending beyond the receptive field of the injured nerve. PB neurons recorded from rats with CCI-ION displayed amplified activity, manifesting as significantly longer responses to sensory stimuli, compared to shams. These findings suggest that chronic neuropathic pain involves PB hyperactivity.
臂旁(PB)复合体在情感/情绪性疼痛通路中介导上行伤害性信号传导和下行疼痛调制信息。我们假设PB功能亢进会影响大鼠三叉神经损伤后的慢性疼痛行为。使用眶下神经慢性压迫损伤(CCI-ION)模型诱导神经性疼痛后,大鼠表现出疼痛的自发指标和机械性痛觉过敏,且超出了受损神经的感受野。与假手术组相比,从CCI-ION大鼠记录的PB神经元显示出活动增强,表现为对感觉刺激的反应明显延长。这些发现表明慢性神经性疼痛涉及PB功能亢进。