Full-length tropomyosin-related kinase B expression in the brainstem in response to persistent inflammatory pain.

Supraspinal descending pathways from the periaqueductal gray and rostral ventromedial medulla dynamically modulate nociceptive transmission in the spinal dorsal horn. We examined the expression of the brain-derived neurotrophic factor receptor trkB in response to inflammation. No difference was observed in the number of neurons expressing trkB in the periaqueductal gray or rostral ventromedial medulla 3 h after inflammation; however, by 24 h, there was a significant increase in trkB expression in the periaqueductal gray (P < 0.05) and rostral ventromedial medulla (P < 0.05), compared with naïve levels, which persisted to 7 days and returned to naïve levels by 21 days. These results demonstrate a temporal increase in the number of cells expressing trkB in response to persistent inflammation, suggesting a role for trkB signaling in activity-dependent plasticity in the pain modulatory circuitry.