Acute autonomic dysreflexia (AD) is a reaction of the autonomic (involuntary) nervous system to overstimulation. It is characterised by severe paroxysmal hypertension (episodic high blood pressure) associated with throbbing headaches, profuse sweating, nasal stuffiness, flushing of the skin above the level of the lesion, bradycardia, apprehension and anxiety, which is sometimes accompanied by cognitive impairment.
My friend Matt Ramer and his team at University of British Columbia use our antibodies as markers for sensory neurons. In this important study they use our
TRPV1 (Neuromics, Edina, MN, USA;
1:2,000)...
Substance P (Neuromics, 1:1,000) and β-III-tubulin (Neuromics; 1:500) to label neuronal profiles in the DRG:
Leanne M. Ramer, A. Peter van Stolk, Jessica A. Inskip,
Matt S. Ramer and Andrei V. Krassioukov. Plasticity of TRPV1-expressing sensory
neurons mediating autonomic dysreflexia following spinal cord injury.
DOI=10.3389/fphys.2012.00257.
Highlights: Spinal cord injury (SCI) triggers profound changes in visceral and somatic
targets of sensory neurons below the level of injury. Despite this, little is
known about the influence of injury to the spinal cord on sensory ganglia. One
of the defining characteristics of sensory neurons is the size of their cell
body: for example, nociceptors are smaller in size than mechanoreceptors or
proprioceptors. In these experiments, we first used a comprehensive
immunohistochemical approach to characterize the size distribution of sensory
neurons after high- and low-thoracic SCI. Male Wistar rats (300 g) received a
spinal cord transection (T3 or T10) or sham-injury. At 30 days post-injury,
dorsal root ganglia (DRGs) and spinal cords were harvested and analyzed
immunohistochemically. In a wide survey of primary afferents, only those
expressing the capsaicin receptor (TRPV1) exhibited somal hypertrophy after T3
SCI. Hypertrophy only occurred caudal to SCI and was pronounced in ganglia far
distal to SCI (i.e., in L4-S1 DRGs). Injury-induced hypertrophy was accompanied
by a small expansion of central territory in the lumbar spinal dorsal horn and
by evidence of TRPV1 upregulation. Importantly, hypertrophy of TRPV1-positive
neurons was modest after T10 SCI. Given the specific effects of T3 SCI on
TRPV1-positive afferents, we hypothesized that these afferents contribute to
autonomic dysreflexia (AD). Rats with T3 SCI received vehicle or capsaicin
via intrathecal injection at 2 or 28 days post-SCI; at 30 days, AD was
assessed by recording intra-arterial blood pressure during colo-rectal
distension (CRD). In both groups of capsaicin-treated animals, the severity of
AD was dramatically reduced.
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