by Victor Chaban, Li Jichang, et al.
July 27, 2008
In women, clinical studies suggest that pain syndromes such as irritable bowel syndrome and interstitial cystitis [painful bladder], which are associated with visceral hyperalgesia [internal organs' increased pain sensitivity], are often comorbid with endometriosis and chronic pelvic pain.
One of the possible explanations for this phenomenon is viscerovisceral cross-sensitization, in which increased nociceptive [pain signaling] input from an inflamed pelvic organ sensitizes neurons that receive convergent input to the same dorsal root ganglion (DRG) from an unaffected visceral organ. [A DRG is a group of nerve cells located along a spinal nerve that monitors pain and relays information into the spinal cord so it can be analyzed by the brain.]
Nociception induces up-regulation of cellular mechanisms such as phosphorylated extracellular signal-regulated kinase (pERK) and substance P (SP), neurotransmitters associated with induced pain sensation.
The purpose of this study was to determine, in a rodent model, whether uterine inflammation increased the number of pERK- and SP-positive neurons that received input from both the uterus and the colon.
Cell bodies of colonic and uterine DRG were retrogradely labeled with fluorescent tracer dyes microinjected into the colon/rectum and into the uterus. Ganglia were harvested for fluorescent microscopy to identify positively stained neurons. Approximately 6% of neurons were colon specific and 10% uterus specific.
Among these uterus- or colon-specific neurons, up to 3-5% of DRG neurons in the lumbosacral neurons (L1-S3 levels) received input from both visceral organs.
Uterine inflammation increased the number of pERK- and SP-immunoreactive DRG neurons innervating specifically colon, or innervating specifically uterus, and those innervating both organs.
These results suggest that a localized inflammation activates primary visceral afferents, regardless of whether they innervate the affected organ [supply it with nerves]. This visceral sensory integration in the DRG may underlie the observed comorbidity of female pelvic pain syndromes.
Source: Journal of Neuroscience Research, online May 2008. PMID: 18478547, by Li J, Micevych P, McDonald J, Rapkin A, Chaban V. Department of Anesthesiology, Harbor UCLA Medical Center; Departments of Neurobiology and Obstetrics/Gynecology, David Geffen School of Medicine, University of California, Los Angeles; Department of Biomedical Sciences, Charles Drew University of Medicine and Science, Los Angeles, California, USA. [E-mail: Victor Chaban victorchaban@cdrewu.edu]
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