Abstract
Cardiovascular dysfunction usually occurs after high thoracic and cervical spinal
cord injury (SCI). The disruption of supraspinal vasomotor pathways (SVPs) results
in the loss of bulbospinal regulation of sympathetic preganglionic neurons, leading
to hypotension and compensatory tachycardia at rest. Episodic autonomic dysreflexia
can develop upon sensory stimulation below the level of injury. In rodents, the precise
spatial distribution of SVPs in the spinal cord originating from the rostral ventrolateral
medulla (RVLM) has not been fully defined. To facilitate future studies of axon regeneration
to regain cardiovascular control, we injected biotinylated dextran amine (BDA) bilaterally
into the RVLM to anterogradely trace SVPs in Fischer 344 (F344) rats. Three weeks
later, BDA-labeled descending projections were predominantly localized within the
dorsolateral funiculus throughout the cervical and thoracic spinal segments as expected.
Additionally, BDA-labeled fibers were also observed in ventral white matter. After
a T4 dorsal hemisection to interrupt the dorsolateral funiculus, BDA labeled terminals
originating from the ventral white matter as well as serotonergic projections were
still detected in regions of autonomic nuclei below the injury. Based on these results,
we examined cardiovascular responses after different lesions at spinal level T4, including
lateral or dorsal hemisection, dorsolateral or complete transection. Hemodynamic dysfunction
and autonomic dysreflexia were only elicited in rats with complete T4 transections
when all SVPs were disrupted. Hence, F344 rats with complete T4 transections provide
a reliable model for investigating means to improve cardiovascular functional recovery
after SCI.
Keywords
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Article info
Publication history
Published online: February 27, 2013
Accepted:
February 1,
2013
Received in revised form:
January 3,
2013
Received:
August 15,
2012
Identification
Copyright
Published by Elsevier Inc.