Visceral sensory afferents during disease or following injury often produce vague, diffuse body sensations, and pain referred to somatic targets. Alternatively, injury due to trauma or disease of somatic nerve targets can also lead to referred pain in visceral targets via a somatovisceral reflex. Both phenomenons are thought to be due to convergence of visceral and somatic afferents within the spinal cord. To investigate a potential peripheral influence for referred pain in visceral targets following somatic nerve injury, we examined whether a sciatic nerve injury known to produce hindpaw tactile hyperalgesia alters the frequency of micturition and the sensitivity of bladder-associated sensory neurons to pro-nociceptive chemokines. Adult female Sprague-Dawley rats received injections of cholera toxin B subunit conjugated to 555 into urinary bladder wall to retrogradely label visceral primary afferent neurons. After 7 days, the right sciatic nerve of these animals was subjected to a lysophosphatidylcholine (LPC)-induced focal demyelination injury. Pre- and post-injury tactile sensitivity in the hind paw and micturition frequency were assayed. Animals were allowed to survive for 14-28 days. Lumbosacral and lumbar dorsal root ganglia (DRG) ipsilateral to the nerve injury were acutely dissociated from sham and nerve injured animals. Bladder wall-associated sensory neurons identified via the retrograde marker were assayed for fluxes in intracellular calcium following administration of pro-nociceptive chemokines. The assayed chemokines included monocyte chemoattractant protein-1 (MCP1/CCL2) and stromal cell derived factor-1 alpha (SDF1/CXCL12). LPC nerve injured animals exhibited tactile hyperalgesia and increased micturition frequency for at least 28 days. Focal demyelination of the sciatic nerve also increased the number of injured L(4)L(5) and non-injured L(6)-S(2) bladder-associated sensory neurons that responded to MCP1 and SDF1 when compared with sensory neurons derived from uninjured naive and sham-injured control animals. Taken together, these data suggest that some visceral hypersensitivity states may have a somatic origin. More importantly, nociceptive somatovisceral sensation may be mediated by upregulation of chemokine signaling in visceral sensory neurons
Keywords : Adult,adverse effects,Analysis of Variance,Animals,Calcium,chemically induced,Chemokines,Cholera Toxin,complications,Disease Models,Animal,Electric Stimulation,etiology,Female,Functional Laterality,Ganglia,Spinal,Hyperalgesia,injuries,innervation,Lysophosphatidylcholines,metabolism,Neurons,Afferent,Pain,Pain Threshold,pathology,pharmacology,Rats,Rats,Sprague-Dawley,Receptors,Chemokine,Sciatic Nerve,Sciatic Neuropathy,Sensation,Spinal Cord,Urinary Bladder,, Nerve,Injury,Induces,Functional,Pronociceptive, shingles neuralgia
Date of Publication : 2011 Jun 2
Authors : Foster R;Jung J;Farooq A;McClung C;Ripsch MS;Fitzgerald MP;White FA;
Organisation : Department of Urology, Loyola University Health System, Maywood, IL, USA
Journal of Publication : Neuroscience
Pubmed Link : https://www.ncbi.nlm.nih.gov/pubmed/21458542
The London Spine Unit : Harley Street UK. Specialists in Cutting Edge Technologies for Spinal Surgery
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