Abstract 58: Neuronal Activation of Ras-Related C3 Botulinum Toxin Substrate 1 (Rac1) Improves Post-Stroke Recovery and Axonal Plasticity in Mice
| Autor: | Fan Bu, Weldon J Furr, Louise D. McCullough, Li Qi, Anthony Patrizz, Jun Li, Yashasvee Munshi, Jia-Wei Min |
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| Rok vydání: | 2019 |
| Předmět: |
Advanced and Specialized Nursing
business.industry Regeneration (biology) Neurogenesis RAC1 Plasticity medicine.disease nervous system Post stroke RAS-RELATED C3 BOTULINUM TOXIN SUBSTRATE 1 Medicine Small GTPase Neurology (clinical) Cardiology and Cardiovascular Medicine business Neuroscience Stroke |
| Zdroj: | Stroke. 50 |
| ISSN: | 1524-4628 0039-2499 |
| DOI: | 10.1161/str.50.suppl_1.58 |
| Popis: | Axonal plasticity is critical for functional recovery after stroke. Our previous study suggested that Rac1, a small GTPase, contributes to post-stroke axonal regeneration. However, the specific cellular and molecular mechanisms mediating its effects remain unknown. The two major factors controlling axonal plasticity in the injured brain are the neuronal intrinsic property for outgrowth and astrocytic inhibition of axonal growth. We investigated the selective roles of neuronal and astrocytic Rac1 in post-stroke recovery and axonal regeneration. Stroke was induced by middle cerebral artery occlusion for 60 minutes in 7 to 8 week old male mice. Brain injection of lentivirus encoding Rac1 with neuronal (NSE) or astrocytic (GFAP) promotors was performed 7 days after stroke in wild type mice to overexpress neuronal or astrocytic Rac1. Tamoxifen administration was started 7 days after stroke in Thy1-cre/Rac1 floxed mice to induce genetic deletion of neuronal Rac1. Delayed overexpression of neuronal Rac1 promoted sensorimotor recovery assessed using a single pellet reaching test (% success rate) from 21 to 28 days after stroke (Day 28: GFP control 51.25±4.41 vs. NSE-Rac1 66.67±2.36, n=8-9, p |
| Databáze: | OpenAIRE |
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