Linked Life Data

12588519

Source:http://linkedlifedata.com/resource/pubmed/id/12588519

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2003-2-17
pubmed:abstractText
Oestradiol (E2) induces luteinizing hormone-releasing hormone (LHRH) hypersecretion, thereby triggering LH surge release in ovariectomized (OVX) rats. Neural signals responsible for the surge are marked by a morning increase in LHRH gene expression and an afternoon increase in LHRH release. Evidence suggests that subpopulations of noradrenergic neurones may be responsible for one or both of these signals. To further investigate this issue, we examined effects of E2 on the activity of A1 and A2 noradrenergic neurones, as reflected in changes in tyrosine hydroxylase (TH) mRNA expression, on the day of LH surge release. We then used dual-label in situ hybridization to determine whether E2-induced changes occurred primarily in A1 and A2 subdivisions wherein most noradrenergic neurones expressed oestrogen receptor (ER)alpha and/or ER beta mRNA. We found that in all subdivisions, levels of TH mRNA were higher in E2- than oil-treated rats at 12.00 h. These differences resulted from a decline in TH mRNA expression in oil-treated rats, as well as a rise in levels in E2-treated rats between 10.00 h and 12.00 h. During the afternoon, TH mRNA expression in most A1 and A2 subdivisions peaked at 14.00 h when LH surge release began. However, in all but the middle and caudal A2 subdivisons, levels were similar in E2-treated and control rats at this time. This was attributable to a widespread increase in TH mRNA expression between 12.00 h and 14.00 h in OVX rats. There was no evidence that E2 induced changes in TH mRNA expression preferentially in regions wherein most neurones contained ER alpha or ER beta mRNA. Our findings suggest that E2 activation of middle and caudal A2 neurones, in conjunction with the widespread E2-independent activation of noradrenergic neurones in other subdivisions, may play a role in the induction of LH surge release.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0953-8194
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
296-303
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:12588519-Animals, pubmed-meshheading:12588519-Estradiol, pubmed-meshheading:12588519-Estrogen Receptor alpha, pubmed-meshheading:12588519-Estrogen Receptor beta, pubmed-meshheading:12588519-Female, pubmed-meshheading:12588519-Gene Expression Regulation, Enzymologic, pubmed-meshheading:12588519-In Situ Hybridization, pubmed-meshheading:12588519-Luteinizing Hormone, pubmed-meshheading:12588519-Medulla Oblongata, pubmed-meshheading:12588519-Neurons, pubmed-meshheading:12588519-Norepinephrine, pubmed-meshheading:12588519-Ovariectomy, pubmed-meshheading:12588519-RNA, Messenger, pubmed-meshheading:12588519-Radioimmunoassay, pubmed-meshheading:12588519-Rats, pubmed-meshheading:12588519-Rats, Sprague-Dawley, pubmed-meshheading:12588519-Receptors, Estrogen, pubmed-meshheading:12588519-Tyrosine 3-Monooxygenase
pubmed:year
2003
pubmed:articleTitle
Oestradiol-dependent and -independent modulation of tyrosine hydroxylase mRNA levels in subpopulations of A1 and A2 neurones with oestrogen receptor (ER)alpha and ER beta gene expression.
pubmed:affiliation
Department of Biology, Neuroscience and Behavior Program and Center for Neuroendocrine Studies, University of Massachusetts, MA 01003, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.