growth in humans (Dobkin and Havton, 2004). Although parts of the white matter of the human spinal cord are almost as large as the entire diameter of the rat spinal cord (Figure 3-1), there is no significant difference in the capacity for oligodendrocyte precursor cells to migrate to remyelinate axons in rats and humans.
One of the issues regarding the differences in scale between smaller laboratory animals and humans that has been discussed is the extent to which testing is needed in primate models. Depending on the treatment, it may be advisable to examine the efficacies of some cell therapies in primates. However, there are also limitations in the use of non-human primates for mimicking human responses. For example, some types of monkeys have specific antibodies that can attack and inhibit the survival of human cells. Additionally, the bioavailability and metabolism of anti-rejection drugs in non-human primates and humans differ significantly. Therefore, rodents have frequently been used as the preferred model to study the efficacies of new immunosuppressive agents because of similarities in metabolism between rodents and humans. In addition, experiments are sometimes performed in rabbits and cats, which have larger spinal cords and are also less expensive and easier to maintain than primates. Furthermore, few tests have been developed to assess changes in spinal cord recovery in nonhuman primates. The committee believes that every therapy need not necessarily be tested in primates before clinical trials are performed with humans and that tests with primates be limited to those that will answer questions that are best explored only with non-human primate models.
The promise accorded by the methodical testing of therapies with animal models is beginning to pay off. Scientists have identified numerous inhibitory molecules and receptors that prevent the regeneration of neurons in the spinal cord and have clarified the pathways by which the inhibitory response can be modulated.
Additional resources and tools are still needed in some areas, however. Animal models need to be developed for solid spinal cord injuries, as they account for a significant portion of human spinal cord injuries (Hulsebosch, 2002). Primate models of contusion injury are particularly needed, as well as standard animal models for cervical spinal cord injuries. Furthermore, there is no standard laboratory animal model that spinal cord injury researchers can use to examine fine motor control of the upper extremities or the loss of the sensory modality proprioception, which is responsible for limb position and immediately varying the degree of muscle contraction in response to external stimuli. When individuals with spinal cord injuries lose their proprioception, they are unable to move freely and interact comfort-