Linked Life Data

11311804

Source:http://linkedlifedata.com/resource/pubmed/id/11311804

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-4-20
pubmed:abstractText
Uterine innervation undergoes cyclical remodeling in the adult virgin rat. Previous studies showed that ovariectomy leads to increased uterine sympathetic nerve density, and this can be reduced by estrogen administration. However, the receptor mechanism by which estrogen modulates sympathetic innervation is unknown. The present study assessed the role of the estrogen receptor alpha in establishing levels of uterine innervation by comparing the nerve abundance in mice with a null mutation of the estrogen receptor alpha with those of the wild-type cycling mouse. Immunostaining for total uterine innervation using antibodies against the pan-neuronal marker protein gene product 9.5 showed that nerve numbers in normally cycling wild-type mice were high in diestrus when circulating estrogen is at its nadir, and low at estrus, coincident with high plasma estrogen. Uteri of the estrogen receptor alpha knock-out mice were smaller than those of wild-type mice, but even when corrected for differences in size, total innervation was 188% and 355% greater than that of wild-type mice at diestrus and estrus, respectively. This hyperinnervation is associated with increased numbers of nerves immunoreactive for the noradrenergic enzyme dopamine beta-hydroxylase, without obvious differences in those containing calcitonin gene-related peptide or the vesicular acetylcholine transporter. While estrogen supplementation of the ovariectomized wild-type mice significantly reduced total uterine innervation, neither ovariectomy nor estrogen supplementation affected uterine nerve density in estrogen receptor alpha knock-out mice.We conclude that estrogen acting through the estrogen receptor alpha determines the number of sympathetic nerve terminal branches within uterine smooth muscle target. In mice with low circulating estrogen, or high estrogen but lacking the functional estrogen receptor alpha, the uterus contains abundant sympathetic nerves, whereas estrogen acts via the estrogen receptor alpha to regulate uterine innervation by reducing numbers of intact sympathetic nerves. Although it is not known whether estrogen acts on the target or neuron to initiate these changes, the estrogen receptor alpha apparently plays a major role in the cyclical modulation of uterine sympathetic innervation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
103
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
237-44
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Sympathetic hyperinnervation of the uterus in the estrogen receptor alpha knock-out mouse.
pubmed:affiliation
Department of Molecular and Integrative Physiology, and R. L. Smith Mental Retardation Research Center, University of Kansas Medical Center, 3901 Rainbow Blvd, Kansas City, KS 66160, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.