Spinal Cord Injury (SCI) currently affects more than 250,000 people in the US alone, and approximately 11,000 new injuries are reported annually. SCI is most commonly caused by trauma, such as vehicular accidents, and often results in devastating paraplegia or tetraplegia. Among many points of interest in treating SCI is what happens to myelin post injury. In terms of electrical conduction, myelin sheaths are the insulation to the wire that is the neuron’s axon, and proper myelination is crucial for effective signaling in the nervous system. Previous findings in SCI research show abnormally thin and short myelin near injury site, supporting the current research dogma that oligodendrocytes (OLs), the glial cells that myelinate the central nervous system, undergo complete cell death following initial injury. Due to lack of methodology, little research has been done to support the idea of partial myelin degeneration. My current study seeks to shed light on the question of where the abnormally thin myelin is derived, if it is indeed newly developed, and explores the possibility that thin myelin found by previous researchers is intact degenerating myelin. Pre-labeled myelin in transgenic mice was injected with a Green Fluorescent Protein (GFP)-labeled virus vector, allowing clear visualization of which myelin sheaths are mature and which are newly generated. By histology and confocal microscopy, I will analyze morphology of neural processes and characteristics of myelinating OLs, such as distances between axon internodes and the axon g-ratio (the relationship of axonal diameter to total fiber diameter, a common measure of myelin thickness). If the prevailing research dogma is supported, I expect to find shortened internode lengths and smaller g-ratios in the green myelin. The findings help determine the significance of myelin change post-SCI and is hoped to contribute more effective therapies to improve axon conduction via pharmacological or cell-based approaches.