Altered GABA and somatostatin modulation of proprioceptive feedback after spinal cord injury in lamprey.

While various changes occur after spinal cord lesions, their influence on functional recovery is generally unclear. We have shown changes in proprioceptor and locomotor network properties below lesion sites in the lamprey spinal cord. The proprioceptive system offers a particularly tractable model for analyzing these changes. Here, we have sought evidence for changes in neuromodulatory effects below lesion sites by comparing the effects of gamma-aminobutyric acid (GABA) and somatostatin, both of which are located around the edge cells, on proprioceptive responses in lesioned and unlesioned spinal cords. Exogenously applied GABA significantly reduced or abolished bending-evoked responses in unlesioned animals. In lesioned animals bending-evoked responses were stronger and certain of the effects of exogenously applied GABA were reduced. However, blocking endogenous GABA with bicuculline significantly potentiated responses in lesioned but not unlesioned animals. This suggested that the potentiated responses in lesioned animals were nevertheless associated with stronger tonic GABAergic inhibition. There were significant differences in these effects when lesioned animals were separated on the basis of their degree of recovery: notably, bicuculline only potentiated responses in animals that recovered good locomotor function, suggesting a need for raised endogenous GABA levels. Somatostatin alone did not affect edge cell responses in lesioned or unlesioned animals, but in lesioned animals it reduced and thus further weakened the inhibitory effects of GABA. There are thus multiple changes in sensory modulation in the lesioned spinal cord, and differences in these effects may influence the degree of recovery.