title: Inverse relation between intensity of GFAP expression in the substantia gelatinosa and degree of chronic mechanical allodynia.
abstract: Glial cells are known to have a large impact on neuropathic pain conditions. Within the spinal cord, microglia rapidly respond to peripheral nerve injury, resulting in central sensitization and ultimately in the onset of enhanced pain behaviour. Astroglia respond with a short delay and are thought to contribute to the early maintenance of neuropathic pain. Nevertheless, it is unknown whether the roles of these glial cell types can be influenced by the chronicity of the neuropathology. Here, the persistent responses of astroglia and microglia to peripheral nerve injury within central pain networks in the upper dorsal horn laminae were studied. At 12 weeks after complete sciatic nerve injury, upregulation of glial fibrillary acidic protein (GFAP), but not complement receptor-3, could be detected in laminae II and III. Moreover, it was found that neuropathic animals with a higher degree of mechanical allodynia had a lower intensity of GFAP expression in lamina II (substantia gelatinosa). From these data we conclude that the role of astroglial responses in mechanical allodynia after peripheral nerve injury may be less straightforward as previously thought. Although astroglia are known to play a pro-nociceptive role in early neuropathic pain states, this role may shift to anti-nociception in more chronic pain states.
authors.affiliation: Pain Management and Research Center, Department of Anesthesiology, Academic Hospital Maastricht, Maastricht, The Netherlands. r.deumens@np.unimaas.nl
authors.forename: Ronald
authors.initials: R
authors.lastname: Deumens
authors.forename: Robby J P
authors.initials: RJ
authors.lastname: Jaken
authors.forename: Liesbeth
authors.initials: L
authors.lastname: Knaepen
authors.forename: Inge
authors.initials: I
authors.lastname: van der Meulen
authors.forename: Elbert A J
authors.initials: EA
authors.lastname: Joosten
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000166:cytology / Q000378:metabolism; D015415:Biomarkers / Q000032:analysis / Q000378:metabolism; D002908:Chronic Disease; D004195:Disease Models, Animal; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis / Q000378:metabolism*; D005911:Gliosis / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D006930:Hyperalgesia / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D007150:Immunohistochemistry; D008297:Male; D017628:Microglia / Q000166:cytology / Q000378:metabolism; D009457:Neuroglia / Q000166:cytology / Q000378:metabolism*; D010148:Intractable Pain / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D020671:Posterior Horn Cells / Q000166:cytology / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011951:Receptors, Complement / Q000378:metabolism; D020426:Sciatic Neuropathy / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D013376:Substantia Gelatinosa / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D015854:Up-Regulation / Q000502:physiology
chemical_list: D015415:Biomarkers; D005904:Glial Fibrillary Acidic Protein; D011951:Receptors, Complement