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Persistent headache and pain sensitization after traumatic brain injury is driven by mu-opioid receptor-positive neurons in the rostral ventromedial medulla for both males and females

Chen Q, Sahbaie P, Irvine KA, Clark JD (2026) Persistent headache and pain sensitization after traumatic brain injury is driven by mu-opioid receptor-positive neurons in the rostral ventromedial medulla for both males and females. Research Square doi: 10.21203/rs.3.rs-9890815/v1

Objective: To investigate whether mu-opioid receptor-positive (Oprm+) pain-facilitating neurons are essential for posttraumatic pain behaviors, ongoing vulnerability to postsurgical and headache-like pain, and latent pain sensitization after mild traumatic brain injury in both male and female animals.

Summary: The rostral ventromedial medulla (RVM) is a key output node of the endogenous pain modulation system, which contains mu-opioid receptor-positive (Oprm+) pain-facilitating neurons that are important in chronic pain. Periorbital mechanical sensitivity was used as a headache-related measure, and hindpaw mechanical withdrawal thresholds were used to assess distal pain sensitization. Lesioning these neurons abolished BLS-induced reinstatement of periorbital allodynia at 5 and 9 weeks after injury in both males and females.

Usage: Male and female C57BL/6J mice received microinjection of Dermorphin-SAP (IT-12)) to lesion RMV Oprm+ neurons, or Blank-SAP (IT-21) as controls (1.5 picomoles in 300 nL of phosphate-buffered saline).

Related Products: Dermorphin-SAP / MOR-SAP (Cat. #IT-12), Blank-SAP (Cat. #IT-21)

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