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. 2017 Nov 13;7:15428. doi: 10.1038/s41598-017-15832-5

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Neuroendocrine hypothesis for etiopathogenesis of benign prostatic hyperplasia. (a) In young human male, prostate transition zone is enriched with 5-HT producing neuroendocrine cells. Serotonin is secreted to the epithelium-stroma interface and through activation of 5-Htr1a and 5-Htr1b, both in epithelium and stroma, the expression of AR is decreased. Yet, more testosterone is delivery to prostate, down-regulated AR limits benign prostate growth. (b) In aged human male, transition zone loses 5-HT producing neuroendocrine cells causing a depletion in local 5-HT. As a consequence 5-Htr1a and 5-Htr1b release their inhibition over AR expression. Although with aging the delivery of testosterone to the prostate is decreased the up-regulation of AR induces the development of BPH. 5-HT, serotonin; AR, androgen receptor; DHT, Dihydrotestosterone; NE, neuroendocrine; T, testosterone.