In addition, a greater concentration of the fluorescent tracer would be expected in the more rostral cells along the RMS were the mechanism involved cell mediated or transcellular. This suggests that it is the existence, and to some degree, the structure of the RMS that is necessary, rather than the functionality; i.e. the movement of cells. This makes CLEFMA surgical transection of the structure a desirable method to evaluate its role. Severe reactive astrogliosis with scar formation is likely to occur in the long term as a result of the direct trauma caused by transection. Astrocyte hypertrophy would only be at the beginning stages at twenty minutes, gene up-regulation such as GFAP mRNA takes an hour to be detected, and glial scar formation would take greater than six hours ; however, reactive astrogliosis and scar formation is unlikely to have a significant effect in the short time frame of this study. The earliest time-point at which hypertrophy is detectible in rats is 24 hours after insult, reaching maximal response in 3�C4 days; the human response is further delayed with detection and maximum around 4 days and 2�C3 weeks, respectively. Interestingly, studies using a longer time frame than this study in evaluating the movement of cells after RMS transection, demonstrated PSA-NCAM positive cells penetrating the glial scar. We also cannot discount the possibility that results may be different in genetic models with a dysfunctional RMS, often resulting in olfactory bulb hypoplasia. However, in these models some degree of cellular migration along the RMS is still present; more important, the architecture of the RMS remains intact. Kaneko et al. recently provided evidence suggesting that the Slit1 MMB-4 protein is used by new neurons to form and maintain astrocyte tunnels, as well as alter astrocyte morphology. This model creates RMS dysfunction through structural alteration and the results of repeating this investigation using Slit1 deficient mice would be interesting; however, it is unclear whether the degree of RMS structural disruption in Slit1 deficient mice is comparable to RMS transection.