作者
Shannon Tansley,Ning Gu,Alba Ureña Guzmán,Weihua Cai,Calvin Wong,Kevin C. Lister,Einer Muñoz-Pino,Noosha Yousefpour,R. Brian Roome,Jordyn Heal,Neil Wu,Annie Castonguay,Graham Lean,Elizabeth M. Muir,Artur Kania,Masha Prager‐Khoutorsky,Ji Zhang,Christos G. Gkogkas,James W. Fawcett,Luda Diatchenko,Alfredo Ribeiro‐da‐Silva,Yves De Koninck,Jeffrey S. Mogil,Arkady Khoutorsky
摘要
Activation of microglia in the spinal cord dorsal horn after peripheral nerve injury contributes to the development of pain hypersensitivity. How activated microglia selectively enhance the activity of spinal nociceptive circuits is not well understood. We discovered that after peripheral nerve injury, microglia degrade extracellular matrix structures, perineuronal nets (PNNs), in lamina I of the spinal cord dorsal horn. Lamina I PNNs selectively enwrap spinoparabrachial projection neurons, which integrate nociceptive information in the spinal cord and convey it to supraspinal brain regions to induce pain sensation. Degradation of PNNs by microglia enhances the activity of projection neurons and induces pain-related behaviors. Thus, nerve injury-induced degradation of PNNs is a mechanism by which microglia selectively augment the output of spinal nociceptive circuits and cause pain hypersensitivity.