Use-dependent modulation of inhibitory capacity in the feline lumbar spinal cord.

Abstract

The ability to perform stepping and standing can be reacquired after complete thoracic spinal cord transection in adult cats with appropriate, repetitive training. We now compare GAD(67)A levels in the spinal cord of cats that were trained to step or stand. We confirmed that a complete spinal cord transection at approximately T12 increases glutamic acid decarboxylase (GAD)(67) in both the dorsal and ventral horns of L5-L7. We now show that step training decreases these levels toward control. Kinematic analyses show that this downward modulation is correlated inversely with stepping ability. Compared with intact cats, spinal cord-transected cats had increased punctate GAD(67) immunoreactivity around neurons in lamina IX at cord segments L5-L7. Compared with spinal nontrained cats, those trained to stand on both hindlimbs had more GAD(67) puncta bilaterally in a subset of lamina IX neurons. In cats trained to stand unilaterally, this elevated staining pattern was limited to the trained side and extended for at least 4 mm in the L6 and L7 segments. The location of this asymmetric GAD(67) staining corresponded to the motor columns of primary knee flexors, which are minimally active during standing, perhaps because of extensor-activated inhibitory interneuron projections. The responsiveness to only a few days of motor training, as well as the GABA-synthesizing potential in the spinal cord, persists for at least 25 months after the spinal cord injury. This modulation is specific to the motor task that is performed repetitively and is closely linked to the ability of the animal to perform a specific motor task.