The specific and limited expression of 5A11/Basigin-2 explicitly within photoreceptor cells implies that this glycoprotein plays a fundamental role within the retina. However, its role remains to be determined.

A number of studies have shown that Chondroitinase ABC (Ch’ase ABC) digestion of inhibitory chondroitin sulfate glycosaminoglycans significantly enhances axonal growth and recovery in rodents following spinal cord injury (SCI). Further, our group has shown improved recovery following SCI in the larger cat model. The purpose of the current study was to determine if intraspinal delivery of Ch’ase ABC, following T10 hemisections in adult cats, enhances adaptive movement features during a skilled locomotor task and/or promotes plasticity of spinal and supraspinal circuitry. Here, we show that Ch’ase ABC enhanced crossing of a peg walkway post-SCI and significantly improved ipsilateral hindlimb trajectories and integration into a functional fore-hindlimb coordination pattern. Recovery of these complex movements was associated with significant increases in neurofilament immunoreactivity immediately below the SCI in the ipsilateral white (p=0.033) and contralateral gray matter (p=0.003). Further, the rubrospinal tract is critical in the normal cat during skilled movements that require accurate paw placements and trajectories like those seen during peg walkway crossing. Rubrospinal connections were assessed following fluorogold injections, caudal to the hemisection. Significantly more retrogradely labeled right (axotomized) red nucleus (RN) neurons were seen in Ch’ase ABC-treated (23%) compared to control-treated cats (8%; p=0.032) indicating that a larger number of RN neurons in Ch’ase ABC-treated cats had axons below the lesion level. Thus, following SCI, Ch’ase ABC may facilitate axonal growth at the spinal level, enhance adaptive features of locomotion, and affect plasticity of rubrospinal circuitry known to support adaptive behaviors in the normal cat.

Background and Purpose The natural response to disability in one limb is to learn new ways of using the other limb. This compensatory behavioral strategy after stroke has long been thought to contribute to persistent dysfunction in the paretic limb by encouraging its disuse. Our recent findings suggest that it goes beyond the encouragement of disuse to disrupt neural substrates of paretic limb functional improvements. Methods We overview recent findings from rodent models of chronic upper extremity impairments in which precise control and manipulation of forelimb experiences were used to understand bilateral and interhemispheric contributions to motor functional outcome. Results Skill learning with the less-affected (nonparetic) forelimb promotes neural plasticity in the contralesional motor cortex that subserves its function. At the same time, it exacerbates dysfunction and limits the efficacy of rehabilitative training in the paretic limb. The maladaptive effects of skill learning with the nonparetic forelimb are dependent on callosal connections and contralesional motor cortex, and linked with reduced neural activation of peri-infarct motor cortex during rehabilitative training. Conclusions These findings suggest that learning to rely on the nonparetic body side has the capacity to disrupt functionality in a region of the injured hemisphere that contributes to outcome of the paretic limb. Whether this effect generalizes across injury loci and functional modalities remains to be tested.