1. Home
  2. Knowledge Base
  3. References
  4. Disruption of spinal noradrenergic activation delays recovery of acute incision-induced hypersensitivity and increases spinal glial activation in the rat.

Disruption of spinal noradrenergic activation delays recovery of acute incision-induced hypersensitivity and increases spinal glial activation in the rat.

Arora V, Morado-Urbina C, Aschenbrenner C, Hayashida K, Wang F, Martin T, Eisenach J, Peters C (2016) Disruption of spinal noradrenergic activation delays recovery of acute incision-induced hypersensitivity and increases spinal glial activation in the rat. J Pain 17:190-202. doi: 10.1016/j.jpain.2015.10.009

Summary: A significant percentage of patients who undergo surgery experience prolonged clinically impactful pain, reducing the quality of life and physical function. Disruption of the descending noradrenergic input has been hypothesized to be important to the generation of this type of pain state. Using an acute incision model, the authors administered 5 μg ofAnti-DBH-SAP (Cat. #IT-03) to the L5-L6 interspace of rats. Mouse IgG-SAP (Cat. #IT-18) was used as a control. Lesioned animals demonstrated a significant increase in mechanical hypersensitivity, and a smaller increase in thermal hypersensitivity. This and other results suggest that spinally projecting noradrenergic pathways are necessary for normal recovery from surgical incision, and possibly other types of pain.

Related Products: Anti-DBH-SAP (Cat. #IT-03), Mouse IgG-SAP (Cat. #IT-18)