Abstract
After experimental spinal cord injury (SCI) in rats, autonomic dysreflexia is commonly induced by slightly noxious cutaneous or visceral stimuli. The presence of autonomic dysreflexia is associated with an increase in the afferent fiber arbor area labeled by cholera toxin B or with an anti-CGRP antibody. Our goal was to examine further the sensory afferent input contributing to exaggerated autonomic spinal reflexes and subsequent increases in blood pressure after SCI, typical of autonomic dysreflexia. We observed that changes in blood pressure and heart rate induced by slightly noxious stimuli (2.0-mL balloon colon distension, cutaneous pinch) were increased in magnitude with time after SCI. In contrast, cardiovascular responses induced by non-noxious stimuli (1.0-mL balloon colon distension, light stroking of hair) were relatively constant. We examined substance P–immunoreactive afferent fibers to identify type C, unmyelinated afferent fibers, and Aδ lightly myelinated fibers in superficial and deeper laminae of the dorsal horn, respectively. The area of substance P–immunoreactive fibers was quantified in laminae I–V of the dorsal horn. Analysis revealed no difference in substance P afferent fiber area in laminae I–II, or laminae III–V, between sham-injured and SCI rats. These data suggest that noxious, or innocuous, stimulation induces autonomic dysreflexia without expansion of the central arbors of substance P–immunoreactive sensory neurons. Furthermore, autonomic dysreflexia induced by noxious stimulation increases with time after spinal cord injury.
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