Genetic Deletion of Paired Immunoglobulin-Like Receptor B Does Not Promote Axonal Plasticity or Functional Recovery after Traumatic Brain Injury
| Autor: | Toshiyuki Takai, Shusaku Omoto, Masaki Ueno, Toshihide Yamashita, Soichiro Mochio |
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| Rok vydání: | 2010 |
| Předmět: |
Male
Traumatic brain injury Biology Inhibitory postsynaptic potential Mice Myelin Neuroplasticity medicine Animals Receptors Immunologic Receptor Mice Knockout Neuronal Plasticity Behavior Animal General Neuroscience Motor Cortex Genetic Therapy Recovery of Function Articles General Medicine medicine.disease Spinal cord Nerve Regeneration Mice Inbred C57BL Disease Models Animal Oligodendrocyte-Myelin Glycoprotein medicine.anatomical_structure Animals Newborn nervous system Brain Injuries Corticospinal tract Neuroscience Gene Deletion Motor cortex |
| Zdroj: | The Journal of Neuroscience. 30:13045-13052 |
| ISSN: | 1529-2401 0270-6474 |
| DOI: | 10.1523/jneurosci.3228-10.2010 |
| Popis: | 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 remodelingin 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. |
| Databáze: | OpenAIRE |
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