title: Genetic deletion of paired immunoglobulin-like receptor B does not promote axonal plasticity or functional recovery after traumatic brain injury.
abstract: The rewiring of neural networks is a fundamental step in recovering behavioral functions after brain injury. However, there is limited potential for axonal plasticity in the adult CNS. The myelin-associated proteins Nogo, myelin-associated glycoprotein (MAG), and oligodendrocyte myelin glycoprotein (OMgp) are known to inhibit axonal plasticity, and thus targeting the inhibitory pathways they participate in is a potential means of promoting plasticity and functional recovery. Each of Nogo, MAG, and OMgp interacts with both the Nogo receptor (NgR) and paired immunoglobulin-like receptor B (PirB). Here, we determined whether blocking PirB activity enhances axonal reorganization and functional recovery after cortical injury. We found that axons of the contralesional corticospinal tract sprouted into the denervated side of the cervical spinal cord after unilateral injury of the motor cortex. The extent to which this axonal reorganization occurred was far greater in mice lesioned during early postnatal days than in mice lesioned at an age when myelin had begun to form. This suggests that myelin-associated proteins might limit axonal remodeling in vivo. However, the number of sprouting fibers within either the corticospinal or corticorubral tract was not enhanced in PirB(-/-) mice. Blocking PirB signaling also failed to enhance functional recovery with three motor tests. Our results suggest that blocking the function of PirB is not sufficient to promote axonal reorganization or functional recovery after cortical injury.
authors.affiliation: Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita-shi, Osaka 565-0871, Japan.
authors.forename: Shusaku
authors.initials: S
authors.lastname: Omoto
authors.forename: Masaki
authors.initials: M
authors.lastname: Ueno
authors.forename: Soichiro
authors.initials: S
authors.lastname: Mochio
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Takai
authors.forename: Toshihide
authors.initials: T
authors.lastname: Yamashita
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001522:Behavior, Animal / Q000502:physiology; D001930:Brain Injuries / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy; D004195:Disease Models, Animal; D017353:Gene Deletion; D015316:Genetic Therapy / Q000379:methods; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009044:Motor Cortex / Q000378:metabolism / Q000503:physiopathology; D009416:Nerve Regeneration / Q000235:genetics; D009473:Neuronal Plasticity / Q000235:genetics*; D011971:Receptors, Immunologic / Q000172:deficiency* / Q000235:genetics* / Q000502:physiology; D020127:Recovery of Function / Q000235:genetics*
chemical_list: C105949:Pirb protein, mouse; D011971:Receptors, Immunologic