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Plasticity of lumbosacral propriospinal neurons is associated with the development of autonomic dysreflexia after thoracic spinal cord transection
Journal article   Open access   Peer reviewed

Plasticity of lumbosacral propriospinal neurons is associated with the development of autonomic dysreflexia after thoracic spinal cord transection

Shaoping Hou, Hanad Duale, Adrian A Cameron, Sarah M Abshire, Travis S Lyttle and Alexander G Rabchevsky
Journal of comparative neurology (1911), v 509(4), pp 382-399
01 Aug 2008
PMID: 18512692
url
https://europepmc.org/articles/pmc2536612View
Accepted (AM)Open Access (License Unspecified) Open

Abstract

Afferent Pathways - physiology Animals Antibodies Autonomic Dysreflexia - etiology Autonomic Dysreflexia - physiopathology Biotin - analogs & derivatives Biotin - pharmacology Choline O-Acetyltransferase - metabolism Dextrans - pharmacology Disease Models, Animal Enkephalins - metabolism Female gamma-Aminobutyric Acid - metabolism Glutamic Acid - metabolism Lumbosacral Region - physiopathology Nerve Fibers - physiology Neuronal Plasticity Neurons - physiology Proto-Oncogene Proteins c-fos - drug effects Proto-Oncogene Proteins c-fos - metabolism Rats Rats, Wistar Spinal Cord - physiopathology Spinal Cord Injuries - physiopathology
Complete thoracic (T) spinal cord injury (SCI) above the T6 level typically results in autonomic dysreflexia, an abnormal hypertensive condition commonly triggered by nociceptive stimuli below the level of SCI. Overexpression of nerve growth factor in the lumbosacral spinal cord induces profuse sprouting of nociceptive pelvic visceral afferent fibers that correlates with increased hypertension in response to noxious colorectal distension. After complete T4 SCI, we evaluated the plasticity of propriospinal neurons conveying visceral input rostrally to thoracic sympathetic preganglionic neurons. The anterograde tracer biotinylated dextran amine (BDA) was injected into the lumbosacral dorsal gray commissure (DGC) of injured/nontransected rats immediately after injury (acute) or 2 weeks later (delayed). At 1 or 2 weeks after delayed or acute injections, respectively, a higher density (P < 0.05) of BDA(+) fibers was found in thoracic dorsal gray matter of injured vs. nontransected spinal cords. For corroboration, fast blue (FB) or cholera toxin subunit beta (CTb) was injected into the T9 dorsal horns 2 weeks postinjury/nontransection. After 1 week transport, more retrogradely labeled (P < 0.05) DGC propriospinal neurons (T13-S1) were quantified in injured vs. nontransected cords. We also monitored immediate early gene c-fos expression following colorectal distension and found increased (P < 0.01) c-Fos(+) cell numbers throughout the DGC after injury. Collectively, these results imply that, in conjunction with local primary afferent fiber plasticity, injury-induced sprouting of DGC neurons may be a key constituent in relaying visceral sensory input to sympathetic preganglionic neurons that elicit autonomic dysreflexia after high thoracic SCI.

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Web of Science research areas
Neurosciences
Zoology
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