Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1999-8-17
pubmed:abstractText
Testosterone is the principal gonadal hormone responsible for the masculinization of the rat nervous system. Sex differences in both the ligand and receptor availability may play a role in the process of sexual differentiation. In some brain regions, males express more androgen receptor (AR) messenger RNA (mRNA) than females by postnatal day (PND) 10. Gonadectomy on the day of birth (PND-0) eliminated the sex differences in AR mRNA expression at PND-10, and exogenous testosterone replacement restored this sex difference. Because testosterone can be converted to both androgenic and estrogenic metabolites in the brain, the present experiments were performed to determine whether androgenic or estrogenic metabolites of testosterone are responsible for region-specific regulation of AR mRNA content in the developing rat forebrain. We used a 35S-labeled riboprobe and in situ hybridization to assess relative steady-state levels of AR mRNA in animals killed on PND-10. In the principal portion of the bed nucleus of the stria terminalis (BSTpr) and medial preoptic area (MPO), males gonadectomized on PND-0 and treated daily with dihydrotestosterone propionate (DHTP), a nonaromatizable androgen, had low levels of AR mRNA that were not significantly different from AR mRNA levels in intact females. In contrast, males gonadectomized on PND-0 and treated daily with diethylstilbestrol (DES), a synthetic estrogen, maintained high, male-typical levels of AR mRNA in the BSTpr and the MPO. AR mRNA content in the VMH was not sexually differentiated in PND-10 rats and was unaffected by gonadectomy or hormone replacement. To further assess whether AR mRNA was autologously regulated, neonatal male rats were treated with the androgen receptor antagonist, flutamide. Flutamide at a dose of either 40 microg/day or 300 microg/day had no effect on AR mRNA expression in any area examined. Thus, AR mRNA is up-regulated by estrogen but is not regulated by androgen during the early postnatal period.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
140
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3674-81
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:10433226-Aging, pubmed-meshheading:10433226-Androgens, pubmed-meshheading:10433226-Animals, pubmed-meshheading:10433226-Animals, Newborn, pubmed-meshheading:10433226-Diethylstilbestrol, pubmed-meshheading:10433226-Dihydrotestosterone, pubmed-meshheading:10433226-Female, pubmed-meshheading:10433226-Flutamide, pubmed-meshheading:10433226-Gene Expression Regulation, Developmental, pubmed-meshheading:10433226-In Situ Hybridization, pubmed-meshheading:10433226-Male, pubmed-meshheading:10433226-Orchiectomy, pubmed-meshheading:10433226-Prosencephalon, pubmed-meshheading:10433226-RNA, Messenger, pubmed-meshheading:10433226-Rats, pubmed-meshheading:10433226-Rats, Sprague-Dawley, pubmed-meshheading:10433226-Receptors, Androgen, pubmed-meshheading:10433226-Sex Characteristics, pubmed-meshheading:10433226-Testosterone, pubmed-meshheading:10433226-Transcription, Genetic
pubmed:year
1999
pubmed:articleTitle
Estrogen, but not androgens, regulates androgen receptor messenger ribonucleic acid expression in the developing male rat forebrain.
pubmed:affiliation
Program in Neuroscience, Stritch School of Medicine, Loyola University Chicago, Maywood, Illinois 60153, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.