BACKGROUND: Nogo-A is a myelin-associated neurite outgrowth inhibitory protein that limits elongation of central nerve fibers, neuronal regeneration and plasticity. We investigated the effect of delivering an inhibitory peptide that neutralizes Nogo-A on neuronal recovery following mild cortical contusion injury. METHODS: 41 rats were allocated into the control and NEP1-40 treatment groups. PBS was applied following trauma over the parietal cortex after opening the dura in the control group. NEP1-40 solution was immediately applied following trauma after opening the dura in the treatment group. Each group was further divided into 3 subgroups and sacrificed on the third, eighth, and 21st days after injury. The brains were removed for analysis. RESULTS: Immunohistochemical staining of the injured cortex for pan-cadherin revealed a significant increase in staining in the NEP 1-40 treatment group at the 8th and 21st days after injury. Electron microscopic evaluation revealed better cytoarchitectural preservation in the axons of the animals treated with NEP 1-40. CONCLUSION: We observed improved preservation of injured neurons after topical application of NEP 1-40 following mild cortical injury. Pan-cadherin expression may correlate with the recovery of neurons and axonal bodies. Electron microscopical findings confirmed better preservation of neuronal structures after NEP1-40 treatment. Pan-cadherin is a good marker for neuronal recovery after cortical injury.
BACKGROUND:Nogo-A is a myelin-associated neurite outgrowth inhibitory protein that limits elongation of central nerve fibers, neuronal regeneration and plasticity. We investigated the effect of delivering an inhibitory peptide that neutralizes Nogo-A on neuronal recovery following mild cortical contusion injury. METHODS: 41 rats were allocated into the control and NEP1-40 treatment groups. PBS was applied following trauma over the parietal cortex after opening the dura in the control group. NEP1-40 solution was immediately applied following trauma after opening the dura in the treatment group. Each group was further divided into 3 subgroups and sacrificed on the third, eighth, and 21st days after injury. The brains were removed for analysis. RESULTS: Immunohistochemical staining of the injured cortex for pan-cadherin revealed a significant increase in staining in the NEP 1-40 treatment group at the 8th and 21st days after injury. Electron microscopic evaluation revealed better cytoarchitectural preservation in the axons of the animals treated with NEP 1-40. CONCLUSION: We observed improved preservation of injured neurons after topical application of NEP 1-40 following mild cortical injury. Pan-cadherin expression may correlate with the recovery of neurons and axonal bodies. Electron microscopical findings confirmed better preservation of neuronal structures after NEP1-40 treatment. Pan-cadherin is a good marker for neuronal recovery after cortical injury.