Intrathecal administration of a sub-effective dose of gabapentin (50 μg) with BoNT/A (0.5 U) induced greater inhibition of pain hypersensitivity and NK1 receptor internalization than BoNT/A alone.
It is suggested that targeting this descending pathway may be effective in reducing persistent pain.<b>NEW & NOTEWORTHY</b> It is known that activation of neurokinin-1 (NK-1) receptors in the rostral ventromedial medulla (RVM), a main output area for descending modulation of pain, produces hyperalgesia.
Subsequent to its release, substance P binds to neurokinin-1 (NK-1) receptors on the surface of effector cells and, in addition to being a mediator of pain, it plays an important role in many inflammatory states including asthma, immune-complex-mediated lung injury, experimental arthritis, and inflammatory bowel disease.