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Abstract
Spontaneous recovery after incomplete spinal cord injury (iSCI) can be partially attributed to plasticity between spared suprasegmental and lumbar segmental circuitry. However, very little is known about the mechanisms involved. The goal of this study was to use the H-reflex to better understand the mechanisms of recovery of hindlimb function after iSCI. The plantar muscle H-reflex, an electrical correlate of the stretch reflex, was measured after Mild and Moderate mid-thoracic contusive SCI, and complete transection at 1, 4, and 8wks in adult female Sprague-Dawley rats. At 1wk, all three injury groups displayed H-reflex baseline amplitude that was comparable to uninjured controls, but the H-reflex rate-depression (i.e. decrease in amplitude in response to increased stimulus frequency) was reduced to a similar extent in all three injury groups. At 4wks, Mild and Moderate contusive SCI, but not transection, showed increased baseline amplitude, indicating that spared suprasegmental pathways were responsible for the increased H-reflex amplitude after contusive SCI. Using pharmacological and immunohistochemical methods, I showed that the increased baseline amplitude Mild SCI was associated with increased function and expression of type-2 serotonin receptors. The changes in baseline amplitude were also associated with functional glutamatergic plasticity of the H-reflex as examined by sensitivity to kynurenate antagonism. This functional plasticity was present after transection and Mild SCI, but occurred in opposite directions. Between 4 and 8wks, the H-reflex rate-depression decreased (became abnormal) after Mild SCI, but increased (became more normal) after transection SCI. Since Mild SCI animals at 4wks have recovered weight-supported locomotion whereas the transected animals have not, this difference in change of rate-depression between Mild and transection SCI could be attributed to differences in hindlimb sensory input between these two groups due to differences in their recovery of hindlimb function. In conclusion, the distal plasticity associated with hindlimb recovery after iSCI involved a complex interaction between spared suprasegmental and segmental circuitry that resulted in functional changes in the processing of primary afferent information. These functional changes included increased recruitment of motoneurons in response to primary afferent input, which may be involved in spontaneous recovery of hindlimb function after iSCI.
