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Acute and chronic estrogen supplementation decreases uterine sympathetic innervation in ovariectomized adult virgin rats

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dc.contributor.authorZoubina, E. V.
dc.contributor.authorMize, A. L.
dc.contributor.authorAlper, R. H.
dc.contributor.authorSmith, P. G.
dc.date.accessioned2020-09-16T17:46:55Z
dc.date.available2020-09-16T17:46:55Z
dc.date.issued2001
dc.description.abstractUterine innervation undergoes substantial reorganization associated with changes in reproductive status. Nerves innervating the uterus are decreased in pregnancy and puberty, and even the normal rodent estrous cycle is characterized by fluctuations in numbers of myometrial nerve fibers. During the follicular (proestrus/estrous) phase of the estrous cycle, intact nerves are rapidly depleted and then return over the next 2-3 days in the luteal (metestrus/diestrus) phase. We hypothesize that uterine nerve depletion is initiated by increased circulating estrogen in the follicular phase . However, studies have not shown whether estrogen can reduce uterine innervation and, if so, whether the time course is compatible with the rapid changes observed in the estrous cycle. These questions were addressed in the present study. Mature ovariectomized virgin rats received 17-B-estradiol as a single injection (10 .ug/kg s.c.) or chronically from timed-release pellets (0.1 .ug/pellet for 3 weeks sustained release). Total (protein gene-product 9.S-immunoreactive) and sympathetic (dopamine B-hydroxylase-immunoreactive) uterine innervation was assessed quantitatively. Both total and sympathetic innervation was abundant in uterine longitudinal smooth muscle of ovariectomized rats. However, following acute or chronic estrogen administration, total and sympathetic fiber numbers were markedly decreased. This was not due to altered uterine size, as reductions persisted after correcting for size differences. Our results indicate that sympathetic nerves are lost from uterine smooth muscle after estradiol treatment in a manner similar to that seen in the intact animal during estrus and pregnancy. This suggests that the rise in estradiol prior to estrus is sufficient to deplete uterine sympathetic innervation.es
dc.formatapplication/pdfes
dc.format.extent8es
dc.identifier.citationHistology and Histopathology, Vol. 16, n.º 1 (2001)
dc.identifier.issn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/96020
dc.languageenges
dc.publisherF. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histologíaes
dc.relationSin financiación externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectNeuroplasticityes
dc.subjectUteruses
dc.subjectEstrous cyclees
dc.subjectAdrenergices
dc.subjectAutonomices
dc.subject.otherCDU::5 - Ciencias puras y naturales::57 - Biología::576 - Biología celular y subcelular. Citologíaes
dc.titleAcute and chronic estrogen supplementation decreases uterine sympathetic innervation in ovariectomized adult virgin ratses
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.16, nº 4 (2001)