Spinal cord injury reduces the efficacy of pseudorabies virus labeling of sympathetic preganglionic neurons.

The retrograde transsynaptic tracer pseudorabies virus (PRV) is used as a marker for synaptic connectivity in the spinal cord. Using PRV, we sought to document putative synaptic plasticity below a high thoracic (T) spinal cord transection. This lesion has been linked to the development of a number of debilitating conditions, including autonomic dysreflexia. Two weeks after injury, complete T4-transected and/or T4-hemisected and sham rats were injected with PRV-expressing enhanced green fluorescent protein (EGFP) or monomeric red fluorescent protein (mRFP1) into the kidneys. We expected greater PRV labeling after injury because of the plasticity of spinal circuitry, but 96 hours post-PRV-EGFP inoculation, we found fewer EGFP+ cells in the thoracolumbar gray matter of T4-transected compared with sham rats (p < 0.01); Western blot analysis corroborated decreased EGFP protein levels (p < 0.01). Moreover, viral glycoproteins that are critical for cell adsorption and entry were also reduced in the thoracolumbar spinal cord of injured versus sham rats (p < 0.01). Pseudorabies virus labeling of sympathetic postganglionic neurons in the celiac ganglia innervating the kidneys was also significantly reduced in injured versus sham rats (p < 0.01). By contrast, the numbers and distribution of Fluoro-Gold-labeled (intraperitoneal injection) sympathetic preganglionic neurons throughout the sampled regions appeared similar in injured and sham rats. These results question whether spinal cord injury exclusively retards PRV expression and/or transport or whether this injury broadly affects host cell-viral interactions.