A microglial SPP1-ITGB1 feedback loop sustains thalamic hyperexcitability and post-stroke pain.

Microglia-derived SPP1 and ITGB1 signaling sustain thalamic hyperexcitability and chronic post-stroke pain in mice.

• Why it matters: Understanding how acute stroke injury transitions into persistent pain is crucial for developing effective treatments, as current knowledge of glial contributions remains incomplete.
• What they did: The study used genetic and pharmacological methods to show that hemorrhage-induced ATP activates microglial SPP1 expression, which then engages an autocrine ITGB1 loop to maintain pain and hyperexcitability.
• The result: Disrupting the SPP1-ITGB1 pathway alleviates chronic pain, highlighting this axis as a key therapeutic target for refractory central post-stroke pain.