| Literature DB >> 35617374 |
Shannon Tansley1,2, Ning Gu1, Alba Ureña Guzmán1, Weihua Cai1, Calvin Wong1, Kevin C Lister1, Einer Muñoz-Pino3, Noosha Yousefpour4, R Brian Roome5, Jordyn Heal1, Neil Wu1, Annie Castonguay3, Graham Lean6, Elizabeth M Muir7, Artur Kania5,8, Masha Prager-Khoutorsky6, Ji Zhang9,10,11, Christos G Gkogkas12, James W Fawcett13,14, Luda Diatchenko1,10,11, Alfredo Ribeiro-da-Silva4,8,11, Yves De Koninck3,4,11, Jeffrey S Mogil1,2,11, Arkady Khoutorsky1,10,11.
Abstract
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.Entities:
Mesh:
Year: 2022 PMID: 35617374 DOI: 10.1126/science.abl6773
Source DB: PubMed Journal: Science ISSN: 0036-8075 Impact factor: 63.714