alexa Estrogen
ISSN: 2161-0479
Journal of Autacoids and Hormones
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Estrogen Preferentially Acts on Visceral Afferents to Modulate the Nociception

Victor Chaban*
Accelerating Excellence in Translational Science (AXIS), Charles R. Drew University of Medicine and Science and David Geffen School of Medicine, University of California, Los Angeles, USA Victor Chaban
Corresponding Author : Victor Chaban, PhD, MSCR
Associate Director
Accelerating Excellence in Translational Science (AXIS)
Charles R. Drew University
1731 East 120 St.
Los Angeles, CA, USA
E-mail: [email protected]; [email protected]
Received November 01, 2012; Accepted November 02, 2012; Published November 05, 2012
Citation: Chaban V (2012) Estrogen Preferentially Acts on Visceral Afferents to Modulate the Nociception. J Autacoids 2:e120. doi: 10.4172/2161-0479.1000e120
Copyright: © 2012 Chaban V. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Many illnesses affect women and men differently. Functional pain syndromes/disorders are more common in women, and some express themselves with different symptoms. With increased awareness of gender differences in responsiveness to therapies in such diseases as the irritable bowel syndrome (IBS) in gastroenterology; chronic pelvic pain (CPP) and endometriosis in gynecology; interstitial cystitis/painful bladder syndrome (IC/PBS) in urology; fibromyalgia in rheumatology; and others, there has been renewed interest in research of gynecologic factors and their possible relationship to visceral pain. Only a thorough understanding of the mechanism implicated in the development of these disorders can truly contribute to the designing of new and more efficient therapies. Basic and clinical evidence has provided initial insights into visceral pain sensitivity, perception, and responsivity. 17β-estradiol (E2), the most potent estrogen of a group of endogenous estrogen steroids may be a causative factor inducing inflammation that contributes to the in visceral pain. Moreover, clinical presentations of functional syndromes often lack a specific pathology in the affected organ but may respond to a viscero-visceral cross-sensitization in which increased nociceptive input from an inflamed organ (i.e., uterus) sensitizes neurons that receive convergent input from an unaffected organ (i.e., colon or bladder). The site of visceral cross-sensitivity is unknown but we hypothesize that viscero-visceral cross-sensitization occurs in the dorsal root ganglion (DRG) where it is modulated by E2.
The cell bodies of primary visceral spinal afferent neurons are located in the lumbosacral (L1-S1) DRGs that transmit information about chemical or mechanical stimulation from the periphery to the spinal cord. Nociceptors are small to medium size DRG neurons whose peripheral processes detect potentially damaging physical and chemical stimuli. ATP and capsaicin have emerged as putative signals for visceral pain. ATP is released by distention of the viscera and tissue damage [1]. Visceral nociceptive capsaicin-sensitive C-fibers are activated by ATP and excitatory amino acids that are released by noxious stimuli from cells in target organs (paracrine action), from afferent terminals themselves (autocrine action, or in sensory ganglia). In our studies, we observed that DRG neurons innervating viscera have a greater (Ca2+) response to subsequent ATP and capsaicin and NMDA stimulation than somatic afferents. These observations indicate that viscerallyspecific neurons express receptors with higher permeability to Ca2+, which can modulate transduction of nociceptive signals and suggest that visceral afferents are functionally different from somatic afferents.
Sex steroids have been suggested as a plausible mechanism of pain regulation (Figure 1). Clinical studies suggest the co-morbidity of functional pain syndromes such as irritable bowel syndrome, painful bladder syndrome, chronic pelvic pain and somatoform disorders approaches 40% to 60% [2]. While a central site of this modulation has been shown previously, our studies suggest a peripheral site, DRG. Based on our data, estrogens have remarkably wide range of functions including modulation of voltage gated calcium channels (VGCC) and TRPV1/P2X3-mediated cascades [3]. Significantly, inflammation may dramatically alter purinoception and capsaicin-induced inflammatorypotentiated TRPV1-mediated response. Gonadal hormones are thoughts as indispensable cornerstones of the normal development and function but it appears that nobody region, no neuronal circuit, and virtually no cell is unaffected by them. Thus, increases awareness toward estrogens appears to be obligatory.
Acknowledgement
This work is supported in part by NIH grants U54MD007598 and NS063939.
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