Suppression of SCI-induced Spasticity Through Inhibition of Glutamate Release

Spinal cord injury induced spasticity (increased muscle tone) in the trunk muscles can significantly hinder the individuals ability to perform transfers, effectively move their head and extremities, decrease the efficacy of their breathing, and lead to development of pressure sores. Currently, gaps exist in our knowledge of what causes spasticity, especially regarding the trunk musculature. These knowledge gaps limited the type and efficacy of treatment options. Glutamate is the major excitatory stimulus to motoneurons, the cells of the spinal cord which turn on muscles. The goals of this proposal are: 1) to determine the effects of spinal transection on the number of glutamatergic inputs to motoneurons below the transection, 2) to correlate these changes with the development of spasticity within tail musculature, which is similar to trunk musculature, and 3) to examine the ability of riluzole and gabapentin, two drugs which selectively interfere with glutamate stimulus, to decrease spasticity within the tail musculature. Results from these experiments will further define the role of glutamate in the development of spasticity and assess the efficacy of two clinically available drugs in the management ofSCI-induced spasticity.