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Visceral‐somatic cross‐sensitization involves increased serotonergic innervation of lumbar dorsal root ganglia (DRG)
Author(s) -
Xia ChunMei,
Yu Sharon J,
Kay Jarren C,
Qiao LiYa
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1075.16
Subject(s) - serotonergic , serotonin , sensitization , endocrinology , visceral pain , 5 ht receptor , immunostaining , dorsal root ganglion , chemistry , medicine , nociception , pathology , neuroscience , receptor , spinal cord , biology , immunology , immunohistochemistry
One of the physiological functions of 5‐hydroxytryptamine (5‐HT) is its modulatory role in pain perception. Release of 5‐HT by serotonergic neurons causes either pro‐ or anti‐nociceptive action by binding to different subtypes of 5‐HT receptors. Here we examined the L5 DRG for serotonergic innervation in two rat models of visceral inflammation‐associated somatic hypersensitivity, namely trinitrobenzenesulfonic acid (TNBS)‐induced colitis and cyclophosphamide (CYP)‐induced cystitis. We found that cystitis at 8h and 48h post CYP injection caused 4 to 5‐fold increases, while colitis at 7 and 21 days caused 1.5 to 2‐fold increases in axonal outgrowth visualized by sucrose‐potassium phosphate‐glyoxylic acid (SPG) staining which was associated with sympathetic sprouting and serotonergic innervation. 5‐HT immunostaining revealed “beaded” fibers – presumably small and regularly spaced varicosities. The number and density of the 5‐HT fibers were time‐dependently increased in DRG of both models. The excitatory effects of 5‐HT was examined by immunostaining of 5‐HT 4 , a G s ‐protein coupled serotonin receptor, and showed marked increases in the number of 5‐HT 4 cells in colitis by 1.5 to 2.3‐fold, and in cystitis by 2‐fold. These results suggest that serotonin/5‐HT 4 ‐mediated sensory hypersensitivity may have a role in visceral inflammation‐induced somatic cross‐sensitization. Grant support: NIH DK077917