Remodeling of uterine innervation

In: Cell and Tissue Research · 2008 · vol. 334(1) , pp. 1–6 · doi:10.1007/s00441-008-0657-x · PMID:18677514 · W2061718936
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This review discusses hypotheses on sympathetic uterine innervation remodeling during the estrous cycle and gestation, noting reduced nerve density with high estrogen and changes in neurotrophins.

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AI-generated deep summary by claude@2026-06, 2026-06-07 · read from full text

This minireview discusses hypotheses for how sympathetic uterine innervation remodels across the rodent estrous cycle and during gestation in humans and rodents, focusing on how hormone levels modulate nerve structure. The authors report that nerve density decreases when estrogen is high in the estrous cycle, with estrogen receptor alpha implicated as a major mediator, and that neurotrophin expression (notably nerve growth factor) varies with steroid levels, influencing nerve fiber survival and growth. A key limitation is that despite extensive work, further studies are needed to clarify mechanisms controlling nerve growth across diverse physiological contexts. Relevance to endometriosis: the review references uterine innervation changes after hysterectomy in chronic pelvic pain with and without endometriosis, though its main focus is general remodeling of uterine sympathetic innervation.

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Abstract

This minireview reports current hypotheses concerning the remodeling of sympathetic innervation in rodent and human uterus during the estrous cycle and gestation. Neural modulation in this organ is related to sexual hormone concentrations, and a reduction in nerve density is observed when estrogen levels are high during the estrous cycle. Estrogen receptor alpha is considered to be the major receptor mediating the action of estrogen. In the uterus, the expression of neurotrophins, such as nerve growth factor, which are involved in the survival and growth of nerve fibers, changes in response to steroid levels. Despite much research, further studies are necessary to clarify various aspects of nerve growth control under diverse physiological conditions. These studies could be of importance, since alterations of the biological mechanisms of uterus innervation may play significant roles in various pathologies, such as infertility and spontaneous abortion.
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Abstract

This minireview reports current hypotheses concerning the remodeling of sympathetic innervation in rodent and human uterus during the estrous cycle and gestation. Neural modulation in this organ is related to sexual hormone concentrations, and a reduction in nerve density is observed when estrogen levels are high during the estrous cycle. Estrogen receptor alpha is considered to be the major receptor mediating the action of estrogen. In the uterus, the expression of neurotrophins, such as nerve growth factor, which are involved in the survival and growth of nerve fibers, changes in response to steroid levels. Despite much research, further studies are necessary to clarify various aspects of nerve growth control under diverse physiological conditions. These studies could be of importance, since alterations of the biological mechanisms of uterus innervation may play significant roles in various pathologies, such as infertility and spontaneous abortion. Similar content being viewed by others

References

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Acknowledgements

We are indebted to Dr. F. Orlando (INRCA, Ancona, Italy) for support and advice. Author information Authors and Affiliations Corresponding author Additional information This review is dedicated to Prof. Enrico Reale (Hannover, Germany), an outstanding scientist and teacher, in memory of his friendship and generous support of our work. A. Frontini and C. Latini equally contributed to this work. Funding was provided by the Polytechnic University of Marche, grants 2006–2007 (to M.M., D.M., and M.C.). Rights and permissions About this article Cite this article Latini, C., Frontini, A., Morroni, M. et al. Remodeling of uterine innervation. Cell Tissue Res 334, 1–6 (2008). https://doi.org/10.1007/s00441-008-0657-x Received: Accepted: Published: Issue date: DOI: https://doi.org/10.1007/s00441-008-0657-x

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