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Intraspinal sprouting of unmyelinated pelvic afferents after complete spinal cord injury is correlated with autonomic dysreflexia induced by visceral pain
Journal article   Open access   Peer reviewed

Intraspinal sprouting of unmyelinated pelvic afferents after complete spinal cord injury is correlated with autonomic dysreflexia induced by visceral pain

Shaoping Hou, Hanad Duale and Alexander G. Rabchevsky
Neuroscience, v 159(1), pp 369-379
24 Dec 2008
PMID: 19146928
url
https://europepmc.org/articles/pmc3546483View
Accepted (AM)Open Access (License Unspecified) Open

Abstract

cholera toxin subunit beta distal colon neuronal plasticity pelvic primary afferent
Autonomic dysreflexia is a potentially life-threatening hypertensive syndrome following high thoracic (T) spinal cord injury (SCI). It is commonly triggered by noxious pelvic stimuli below the injury site that correlates with increased sprouting of primary afferent C-fibers into the lumbosacral spinal cord. We have recently demonstrated that injury-induced plasticity of lumbosacral propriospinal neurons, which relay pelvic visceral sensations to thoracolumbar sympathetic preganglionic neurons, is also correlated with the development of this syndrome. To determine the phenotype of pelvic afferent fiber sprouts after SCI, cholera toxin subunit beta (CTb) was injected into the distal colon 2 weeks post T4 transection/sham to label colonic visceral afferents. After 1 week transport, the lumbosacral spinal cords were cryosectioned and immunohistochemically stained for CTb, the nociceptive-specific marker calcitonin gene-related peptide (CGRP), and the myelinated fiber marker RT97. Quantitative analysis showed that the density of CGRP + afferent fibers was significantly increased in the L6/S1 dorsal horns of T4-transected versus sham rats, whereas RT97 + afferent fiber density showed no change. Importantly, CTb-labeled pelvic afferent fibers were co-localized with CGRP + fibers, but not with RT97 + fibers. These results suggest that the sprouting of unmyelinated nociceptive pelvic afferents following high thoracic SCI, but not myelinated fibers, contributes to hypertensive autonomic dysreflexia induced by pelvic visceral pain.

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