Pain-related behavioral and electrophysiological actions of dynorphin A (1-17)

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.

Automated summary

Dynorphin A (1-17) (DynA17) has been identified as a key regulator of chronic pain, affecting both the sensory and affective dimensions. Blocking the increases of DynA17 in spinal and supraspinal areas related to chronic pain has therapeutic benefits in preclinical models. This report investigates the cellular physiological effects of DynA17 and how intrathecal administration modifies the periaqueductal gray, a crucial node in the pain axis.