Department of Anesthesiology and Critical Care Medicine, University of New Mexico School of Medicine, Albuquerque, NM, USA.
Mol Pain. 2023 Jan-Dec;19:17448069231186592. doi: 10.1177/17448069231186592.
Dynorphin A (1-17) (DynA17) has been identified as a key regulator of both sensory and affective dimensions of chronic pain. Following nerve injury, increases in DynA17 have been reported in the spinal and supraspinal areas involved in chronic pain. Blocking these increases provides therapeutic benefits in preclinical chronic pain models. Although heavily characterized at the behavioral level, how DynA17 mediates its effects at the cellular physiological level has not been investigated. In this report, we begin to decipher how DynA17 mediates its direct effects on mouse dorsal root ganglion (DRG) cells and how intrathecal administration modifies a key node in the pain axis, the periaqueductal gray These findings build on the plethora of literature defining DynA17 as a critical neuropeptide in the pathophysiology of chronic pain syndromes.
强啡肽 A（1-17）（DynA17）已被确定为慢性疼痛的感觉和情感维度的关键调节剂。在神经损伤后，已在涉及慢性疼痛的脊髓和脊髓上区域中报告了 DynA17 的增加。在临床前慢性疼痛模型中，阻断这些增加可提供治疗益处。尽管在行为水平上得到了广泛的描述，但 DynA17 如何在细胞生理水平上发挥其作用尚未得到研究。在本报告中，我们开始阐明 DynA17 如何介导其对小鼠背根神经节（DRG）细胞的直接作用，以及鞘内给药如何修饰疼痛轴中的关键节点，即中脑导水管周围灰质。这些发现建立在大量文献的基础上，这些文献将 DynA17 定义为慢性疼痛综合征病理生理学中的关键神经肽。
