Collapsin response mediator protein 2 (CRMP2) is a microtubule-associated phosphoprotein in the mammalian CNS. It has multifunctional properties and is known to influence neuronal cytoskeleton integrity, a function that is inhibited following phosphorylation after injury. Importantly, preventing phosphorylation is reported to stabilise axons and promote neuronal survival after trauma. In this pilot study, CRMP2’s neuroprotective capacity was investigated following a moderate cervical C6/7 hemi-lateral contusion spinal cord injury (SCI) in anaesthetised adult female F344 rats. Corticospinal neurons were transduced immediately after SCI by injecting bi-cistronic adeno-associated viral vectors (AAV1) expressing a mutated phospho-resistant form of CRMP2 (mCRMP2^GFP) (n=4) or AAV1^mCherry in control rats (n=4) into contralateral forelimb sensorimotor cortex. Functional deficits and improvements were analysed for 8 weeks with behavioural tests. Morphology of corticospinal tract (CST) axons was compared between treatment groups by injecting biotinylated dextran amine into the same previously transduced region of cortex. Rats were perfused two weeks thereafter (D56 after SCI). Despite demonstrating significant functional deficits associated with CST impairment there were no significant differences between treatment and control groups. Qualitatively, we observed fewer degenerative CST axons, increased microglia infiltration and smaller cysts (p>0.05) near the injury in mCRMP2 treated rats. However, there was considerable variability, presumably from inconsistent damage sustained by the CST during the injury. In summary, transduction of mCRMP2 with AAV1 into the sensorimotor cortex of the rat brain can successfully target corticospinal neurons and their axons, providing a potential avenue to further explore the neuroprotective effects of mCRMP2 after SCI.