{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T19:38:31Z","timestamp":1790797111361,"version":"4.1.0"},"reference-count":58,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2015,12,12]],"date-time":"2015-12-12T00:00:00Z","timestamp":1449878400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["31100837"],"award-info":[{"award-number":["31100837"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neurogastroenterology Motil"],"published-print":{"date-parts":[[2016,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Estrogen may regulate gastrointestinal motor functions, but the mechanism(s) is not totally understood. Here, we investigated whether G protein\u2010coupled estrogen receptor (<jats:styled-content style=\"fixed-case\">GPER<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">GPR<\/jats:styled-content>30) was involved in regulating colonic motor functions and explored the underlying physiological mechanisms.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Adult female C57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>\/6 mice were used. The expression and localization of <jats:styled-content style=\"fixed-case\">GPER<\/jats:styled-content> were examined by <jats:styled-content style=\"fixed-case\">RT<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PCR<\/jats:styled-content>, western blot, and immuno\u2010labeling. The role of <jats:styled-content style=\"fixed-case\">GPER<\/jats:styled-content> in modulating colonic motor functions was assessed by the bead propulsion test <jats:italic>in vivo<\/jats:italic> and organ bath experiments <jats:italic>in vitro<\/jats:italic>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key Results<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">GPER<\/jats:styled-content> was expressed in colonic myenteric neurons. The colonic transit time (<jats:styled-content style=\"fixed-case\">CTT<\/jats:styled-content>) in proestrus and estrus was significantly longer than that in diestrus. <jats:italic>In vivo<\/jats:italic> treatment with the selective <jats:styled-content style=\"fixed-case\">GPER<\/jats:styled-content> blocker G15 significantly shortened <jats:styled-content style=\"fixed-case\">CTT<\/jats:styled-content> in proestrus and estrus. In ovariectomized mice, acute estrogen supplementation increased <jats:styled-content style=\"fixed-case\">CTT<\/jats:styled-content>, which could be abolished by G15 co\u2010administration. The <jats:styled-content style=\"fixed-case\">GPER<\/jats:styled-content> agonist G\u20101 caused a concentration\u2010dependent inhibition of carbachol \u2010induced circular muscle strips contraction, which was abolished by tetrodotoxin and the neuronal nitric oxide synthase (<jats:styled-content style=\"fixed-case\">nNOS<\/jats:styled-content>) inhibitor <jats:italic>N<\/jats:italic>\u2010propyl\u2010<jats:sc>l<\/jats:sc>\u2010arginine. G\u20101 stimulated <jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content> production in isolated longitudinal muscle myenteric plexus and cultured myenteric neurons, which was dependent on <jats:styled-content style=\"fixed-case\">nNOS<\/jats:styled-content>. Immunofluorescence labeling showed co\u2010localization of <jats:styled-content style=\"fixed-case\">GPER<\/jats:styled-content> with <jats:styled-content style=\"fixed-case\">nNOS<\/jats:styled-content> in the myenteric plexus.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions &amp; Inferences<\/jats:title><jats:p>We suggest that activation of <jats:styled-content style=\"fixed-case\">GPER<\/jats:styled-content> exerts an inhibitory effect on colonic motility by promoting <jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content> release from myenteric nitrergic nerves. These results raise a possibility that <jats:styled-content style=\"fixed-case\">GPER<\/jats:styled-content> may be involved in mediating the inhibitory effect of estrogen on colonic motor functions, via a non\u2010genomic, neurogenic mechanism.<\/jats:p><\/jats:sec>","DOI":"10.1111\/nmo.12743","type":"journal-article","created":{"date-parts":[[2015,12,12]],"date-time":"2015-12-12T15:13:06Z","timestamp":1449933186000},"page":"432-442","source":"Crossref","is-referenced-by-count":46,"title":["G protein\u2010coupled estrogen receptor is involved in modulating colonic motor function via nitric oxide release in C57<scp>BL<\/scp>\/6 female mice"],"prefix":"10.1111","volume":"28","author":[{"given":"Y.","family":"Li","sequence":"first","affiliation":[{"name":"Department of Pathophysiology Medical School Shandong University Jinan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of 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